Cockayne syndrome is a rare genetic condition that affects growth and the nervous system. Many people with Cockayne syndrome have poor weight gain, short stature, vision and hearing problems, and learning or movement difficulties. Signs usually begin in infancy or early childhood and tend to worsen over time. Care is supportive and may include nutrition support, physical and occupational therapy, hearing aids, glasses, and regular monitoring. The outlook varies by type, and severe forms can shorten lifespan, but care teams focus on comfort, function, and prevention of complications.
Overview
Cockayne syndromeSymptoms
Cockayne syndrome causes poor growth, small head size, and delayed development. People often have extreme sun sensitivity, hearing and vision loss, and problems with movement, feeding, or learning.
Outlook and prognosis
Many living with Cockayne syndrome face progressive challenges with growth, hearing, vision, movement, and learning. Care focuses on comfort, nutrition, mobility, and preventing infections, which can meaningfully improve daily life. Lifespan varies by type; earlier-onset forms progress faster.
Causes and risk factors
Cockayne syndrome results from inherited mutations in DNA-repair genes (usually ERCC6/ERCC8) and is autosomal recessive. Risk is higher when both parents are carriers, including in consanguineous families. UV light can aggravate features but doesn’t cause the condition.
Genetic influences
Genetics is central in Cockayne syndrome: it’s caused by inherited changes in DNA repair genes, usually ERCC6 or ERCC8. Most cases follow an autosomal recessive pattern. Variations in these genes influence age at onset, severity, and specific features.
Diagnosis
Diagnosis of Cockayne syndrome relies on recognizable clinical features and poor growth, then confirmation with genetic testing of ERCC6 or ERCC8. Brain MRI and other imaging may support the genetic diagnosis of Cockayne syndrome.
Treatment and drugs
Treatment for Cockayne syndrome focuses on comfort, growth, and function. Care often includes nutrition support, sun protection, physical and occupational therapy, hearing and vision aids, dental care, and careful management of infections and seizures. A coordinated team tailors plans as needs change.
Symptoms
Families often notice slow growth, feeding challenges, and a strong sensitivity to sunlight in early childhood. These early features of Cockayne syndrome can affect mealtimes, time outdoors, and play. Features vary from person to person and can change over time. Hearing and vision changes, joint stiffness, and learning delays are also common.
Height and weight often increase more slowly than expected for age. This can mean wearing smaller sizes and needing close monitoring at checkups. Doctors may discuss higher-calorie meals or supplements.
Clinicians call this microcephaly, which means a head size smaller than expected for age. In everyday life, hats and helmet sizes may be smaller than peers. Doctors track head growth with a tape measure over time.
Babies may tire during feeds or have trouble coordinating sucking and swallowing. Reflux or gagging can make meals stressful. Some families use thickeners, special nipples, or a feeding tube to support nutrition.
Sitting, walking, and talking can take longer to develop. Many children benefit from physical, occupational, and speech therapy. Progress is still possible with practice and support.
How people usually first notice Cockayne syndrome?
Parents and clinicians often first notice Cockayne syndrome in infancy when a baby isn’t gaining weight or growing as expected, even with good feeding, and when the head size stays small for age. As months go by, many develop sun-sensitive skin with easy burning after brief sun exposure, along with delayed milestones such as sitting or walking, and a thin, “cachectic” look despite adequate nutrition. These first signs of Cockayne syndrome may be picked up at routine well-baby visits, where slowed growth, developmental delays, and photosensitivity prompt genetic evaluation.
Types of Cockayne syndrome
Cockayne syndrome has a few well-recognized clinical variants that mainly differ in age at onset and how quickly features progress. These variants reflect differences in the same DNA-repair pathway, most often involving changes in the ERCC6 (CSB) or ERCC8 (CSA) genes. People may notice different sets of symptoms depending on their situation. When learning about the types of Cockayne syndrome, it helps to know that earlier onset usually goes with faster progression and more medical needs over time, and that types of Cockayne syndrome are defined by these patterns rather than by separate causes.
Type I (classic)
Symptoms usually appear in early childhood with poor growth, sensitivity to sunlight, and developmental delays. Hearing and vision problems often follow, with gradual loss of skills over time. Life expectancy is reduced, but some reach adolescence or adulthood.
Type II (severe early-onset)
Features are present at birth or in the first months, with very slow growth and marked feeding and movement challenges. Neurologic problems are pronounced and progression is rapid. Most children have a shorter lifespan, often limited to early childhood.
Type III (milder)
Onset tends to be later with milder growth and learning concerns. Sun sensitivity may be present but other features progress more slowly. Many maintain more independence into adulthood.
XP-CS overlap
This variant combines Cockayne features with xeroderma pigmentosum–like skin changes. People have extreme sun sensitivity with a higher risk of skin cancers, alongside neurodevelopmental issues seen in Cockayne syndrome. Regular skin surveillance is essential.
What genetics can tell you about symptoms
Some people with Cockayne syndrome who carry ERCC6 changes tend to show earlier growth failure, light sensitivity, and hearing loss, while ERCC8 changes often bring more severe developmental delays. Both genes affect DNA repair, which raises sensitivity to sun and speeds aging-like features.
Causes and risk factors
Cockayne syndrome is caused by harmful changes in the ERCC6 or ERCC8 genes that help repair DNA, usually inherited but sometimes new. Some risks are written in our DNA, passed down through families. It follows an autosomal recessive pattern, so two carrier parents have a 25% (1 in 4) chance of an affected child with each pregnancy. Risk factors for Cockayne syndrome include having two carrier parents, a known family history, or parents who are related by blood. Sunlight and other ultraviolet exposure can make early symptoms of Cockayne syndrome worse, but they do not cause the condition, and lifestyle changes cannot prevent it.
Environmental and biological risk factors
Understanding what raises the chance of a child being born with Cockayne syndrome can help families plan and ask focused questions. Doctors often group risks into internal (biological) and external (environmental). This section highlights environmental risk factors for Cockayne syndrome and the biological influences present before birth. For this condition, biological factors play the main role, and there are no proven day-to-day exposures that cause it.
When parents share close family ties (for example, cousins), the chance of rare conditions appearing in a child goes up. This added risk reflects shared family background, not anything either parent did during pregnancy.
New changes can accumulate in sperm as paternal age increases, which slightly raises the chance of a rare condition in a child. This effect is small and not specific to Cockayne syndrome. Most children born to older fathers are unaffected.
Everyday exposures before or during pregnancy—such as typical air pollution levels, common household products, or usual workplace conditions—are not known to increase the chance of Cockayne syndrome. High-dose medical exposures (like cancer radiation therapy) are managed carefully, and most pregnancies do not involve them. If specific hazards are a concern, discussing them with a prenatal clinician can help put risk in context.
Genetic risk factors
Changes in two DNA repair genes are the main genetic cause of Cockayne syndrome. These inherited changes disrupt a pathway that helps cells fix damage in active genes (known medically as transcription-coupled nucleotide excision repair). Carrying certain risks doesn’t automatically lead to Cockayne syndrome. Genetic testing is typically considered when early symptoms of Cockayne syndrome raise concern, and it can clarify which gene is involved.
ERCC6 (CSB): Changes in this gene are the most common genetic cause of Cockayne syndrome. They impair the cell’s ability to fix DNA damage during active gene use.
ERCC8 (CSA): Variants in this gene also cause Cockayne syndrome. They affect the same DNA repair pathway, with overlap in severity and symptoms.
Autosomal recessive pattern: A child is affected when they inherit two non-working copies of the same gene, one from each parent. Carriers usually have no symptoms.
Carrier parents: If both parents carry a Cockayne syndrome gene change, each pregnancy has a 25% (1 in 4) chance of an affected child. There is also a 50% (1 in 2) chance the child will be a healthy carrier.
Family history: When a sibling or child has Cockayne syndrome, close relatives are more likely to be carriers. Cascade testing can identify who in the family carries the change.
Parental relatedness: When parents are related by blood or share close ancestry, the chance they carry the same rare change increases. This raises the likelihood of having a child with Cockayne syndrome.
Variant severity: Some changes completely stop the gene from working and tend to cause earlier, more severe Cockayne syndrome. Milder changes may be linked with later-onset forms and longer survival.
Compound heterozygosity: Two different non-working changes in the same gene, one from each parent, can also cause Cockayne syndrome. Genetic testing looks for both changes to confirm the diagnosis.
Founder variants: In some families or regions, the same inherited change appears repeatedly due to a shared ancestor. This can make targeted testing more efficient for Cockayne syndrome in those groups.
Lifestyle risk factors
Lifestyle habits do not cause Cockayne syndrome, but daily choices can shape symptoms, comfort, and complications. In this context, there are no lifestyle risk factors for Cockayne syndrome in the causative sense, yet routines can influence skin comfort, growth, mobility, and sensory challenges. Understanding how lifestyle affects Cockayne syndrome helps families prioritize supportive habits without implying blame.
Excess sun exposure can worsen photosensitivity, skin irritation, and eye discomfort. Consistent photoprotection (shade, clothing, sunscreen, UV-blocking glasses) may reduce rashes and light-triggered pain.
Insufficient calories and protein can intensify poor growth, low energy, and muscle loss. High-calorie, nutrient-dense meals and safe feeding strategies can support weight gain and stamina.
Rapid eating or unsafe textures can increase choking and aspiration risk. Slow pacing, upright positioning, and texture modification can improve tolerance and reduce respiratory complications.
Low fluid intake can worsen constipation, kidney strain, and fatigue. Regular hydration supports bowel regularity, skin integrity, and overall comfort.
Risk prevention
Cockayne syndrome is a rare genetic condition you can’t fully prevent once a pregnancy has started, but you can lower the chance of passing it on in future pregnancies and reduce day-to-day complications. Planning options before or early in pregnancy can help families at higher risk make informed choices, and early supportive care can limit problems from sun sensitivity, infections, and poor growth. Even if you can’t remove all risks, prevention can reduce their impact. Spotting early symptoms of Cockayne syndrome and staying on top of routine care often leads to faster support and fewer complications over time.
A genetics professional can explain inheritance, carrier testing, and recurrence chances. They can outline options for future pregnancies and connect you with support.
If Cockayne syndrome runs in your family, a simple blood or saliva test can check if you carry the gene change. Testing partners helps estimate the chance of having an affected child.
In vitro fertilization with preimplantation genetic testing can identify embryos not affected by Cockayne syndrome. This may reduce the chance of passing on the condition.
During pregnancy, tests such as chorionic villus sampling or amniocentesis can check if the baby has Cockayne syndrome. Results can guide planning and early care.
Transmission
Cockayne syndrome is not contagious and cannot be caught or spread through everyday contact. It is inherited in an autosomal recessive way: a child must receive two altered copies of the gene—one from each parent—to develop Cockayne syndrome. People who carry one altered copy usually have no symptoms; when both partners are carriers, each pregnancy has a 25% (1 in 4) chance of a child with Cockayne syndrome, a 50% (1 in 2) chance of a carrier, and a 25% (1 in 4) chance of neither. Rarely, Cockayne syndrome happens due to a new genetic change with no family history; a genetics professional can explain how Cockayne syndrome is inherited in your family.
When to test your genes
Consider genetic testing if a child has unexplained growth failure, photosensitivity, early-onset hearing or vision loss, developmental delay, or neurological regression, especially with a family history of Cockayne syndrome. Test during pregnancy if both parents are known carriers. Earlier confirmation guides care, supportive therapies, and family planning for future pregnancies.
Diagnosis
For many, the first step comes when everyday activities start feeling harder—like sunlight causing stinging skin or school skills not progressing as expected. Cockayne syndrome is usually recognized by a pattern of features such as slow growth, small head size, sensitivity to light, and developmental delays. Doctors confirm the picture with targeted tests that look at genes and, in some cases, how cells handle UV-related damage. Getting a diagnosis is often a turning point toward answers and support. The genetic diagnosis of Cockayne syndrome typically combines clinical evaluation with gene testing to be certain.
Providers look for a consistent pattern—poor growth, small head size, photosensitive skin, and developmental delay. Noting when symptoms began and how they’ve changed over time helps shape the diagnosis.
A detailed family and health history can help connect symptoms across relatives. This can point to an inherited pattern and guide which tests come next.
A blood or saliva test checks for changes in genes called ERCC6 and ERCC8. Finding known disease‑causing variants can confirm the diagnosis of Cockayne syndrome.
In some centers, skin cells may be tested for how they repair UV-related DNA damage. Abnormal repair supports Cockayne syndrome when gene results are unclear.
Stages of Cockayne syndrome
Cockayne syndrome does not have defined progression stages. Symptoms and changes vary widely by subtype and from person to person, so experts describe types (often called type I, II, or III) rather than a step-by-step stage system. Diagnosis relies on the overall pattern—such as early symptoms of Cockayne syndrome like slow growth, developmental delays, and marked sensitivity to sunlight—along with hearing and vision checks and imaging; Different tests may be suggested to help confirm the diagnosis. Genetic testing can confirm the cause and helps plan ongoing care for growth, nutrition, hearing, vision, and skin protection.
Outlook and prognosis
Looking at the long-term picture can be helpful. Many people ask, “What does this mean for my future?”, especially after hearing a diagnosis of Cockayne syndrome. The outlook is not the same for everyone, but this condition is generally serious and shortens life expectancy. Children with the classic, early-onset form often have slow growth, hearing and vision changes, feeding challenges, and increasing difficulty with movement and learning over time. Daily routines often adapt, for example, needing softer foods, mobility aids, and careful sun protection because the skin can be very sensitive to light.
Doctors call this the prognosis—a medical word for likely outcomes. In the most common, early-onset type, many children live into late childhood or the teenage years; in milder, later-onset types, some people reach adulthood, though health issues usually progress. Early symptoms of Cockayne syndrome, such as poor weight gain and delayed milestones, can signal a faster-changing course, and frequent infections or swallowing difficulties can raise health risks. With ongoing care, many people maintain comfort and meaningful routines, especially with proactive nutrition support, eye and hearing care, physical therapy, and seizure management if needed. Serious complications, including lung infections and problems related to swallowing and nutrition, are the most common reasons this condition can shorten life.
Understanding the prognosis can guide planning and help families match care to their goals. Support from friends and family can make day-to-day life safer and more connected, and palliative care teams can focus on comfort at any stage. Genetic testing can sometimes provide more insight into prognosis, since different gene changes can be linked to earlier or later onset. Talk with your doctor about what your personal outlook might look like, and ask about steps that can prevent complications, like vaccination, safe feeding strategies, and early treatment of infections.
Long-term effects
For many, the long-term picture of Cockayne syndrome involves gradual changes in growth, movement, hearing, and vision that shape daily life. Long-term effects vary widely, and they can progress at different speeds even within the same family. Families sometimes look back and recognize early symptoms of Cockayne syndrome, like feeding difficulties and slow growth, that later connect with the long-term picture. Care teams follow these changes over time to guide supports and planning.
Most children grow slowly and remain smaller than peers. Weight gain can be limited even with careful feeding.
Many develop a small head compared with body size. This feature often becomes more noticeable over time in Cockayne syndrome.
Movement can become stiffer and slower. Tasks like walking, climbing stairs, or using utensils may get harder with age.
Wobbliness or unsteady gait can increase. Falls may become more frequent as muscles weaken and reflexes slow.
How is it to live with Cockayne syndrome?
Living with Cockayne syndrome often means weaving medical care into everyday life, with frequent appointments, therapies, and adaptations for vision, hearing, and mobility changes. Many children and adults tire easily, need help with feeding or communication, and rely on protective routines like sun avoidance and careful skin and eye care because their bodies are unusually sensitive to UV light. Families and caregivers become a close care team, adjusting schedules, homes, and expectations while celebrating small milestones and watching for infections or nutrition issues. Support from specialists, early interventions, and community resources can ease daily challenges and help shape days around comfort, connection, and meaningful activities.
Treatment and drugs
Treatment for Cockayne syndrome focuses on easing symptoms, supporting growth and movement, protecting hearing and vision, and preventing complications. There’s no cure yet, so care is usually coordinated by a pediatrician or internist alongside neurology, ophthalmology, audiology, nutrition, dentistry, physical and occupational therapy, and dermatology; your doctor may suggest regular check-ins to adjust the plan as needs change. Common treatments include high-calorie, texture-appropriate nutrition (sometimes with a feeding tube), eye care for cataracts or dry eyes, hearing aids, physical therapy to maintain flexibility and mobility, speech therapy for feeding and communication, sun protection for very sensitive skin, and medicines for pain, stiffness, reflux, constipation, or mood. Surgery may be considered for specific issues like cataracts, severe contractures, or dental problems, while close monitoring helps catch infections, growth concerns, or new neurologic symptoms early. Finding the right therapy can take some time, and supportive care can make a real difference in how you feel day to day.
Non-drug treatment
Non-drug care for Cockayne syndrome focuses on comfort, nutrition, movement, communication, and protecting sensitive skin and eyes. Supportive therapies can help slow functional loss, ease daily routines, and reduce complications. Starting services when early symptoms of Cockayne syndrome appear may preserve abilities for longer. Plans are tailored over time as needs change.
Gentle stretching and positioning can help prevent joint stiffness and contractures. Movement practice and supported standing aim to preserve comfort, balance, and circulation.
Daily living skills are broken into small, achievable steps to maintain independence. Adaptive tools and home setup changes make feeding, dressing, and play easier for children with Cockayne syndrome.
Strategies for safe swallowing can lower the risk of choking and chest infections. Communication therapy builds understanding and expression, using gestures, pictures, or devices when speech is limited.
High-calorie meals, texture changes, and supplemental formulas help with growth and energy. A dietitian can tailor plans for Cockayne syndrome to reduce fatigue and support the immune system.
Your genes may have an impact on how drugs work for you
For Cockayne syndrome, genes can affect how the body handles medicines—how fast a drug is broken down, how strongly cells respond, and how likely side effects appear. Clinicians sometimes adjust drug type or dose based on these inherited differences.
Pharmacological treatments
Medicines for Cockayne syndrome focus on comfort, symptom control, and safety; there is no cure yet. Drugs that target symptoms directly are called symptomatic treatments. Doctors often combine several options and adjust doses as needs change over time. Not everyone responds to the same medication in the same way.
Levetiracetam, lamotrigine, valproate, or clobazam may reduce seizures and help protect daily alertness. Doses are adjusted to balance seizure control with side effects.
Baclofen, tizanidine, or diazepam can loosen tight muscles and ease stiffness. Botulinum toxin injections may help specific muscles that are very tight.
Omeprazole or lansoprazole (proton pump inhibitors) and famotidine (an H2 blocker) can reduce stomach acid and soothe reflux-related discomfort. This may lessen coughing after feeds and improve sleep.
Polyethylene glycol, lactulose, or senna can keep stools soft and more regular. Adequate fluids and fiber remain important alongside these medicines.
Genetic influences
Most people inherit Cockayne syndrome when both parents carry a silent change in the same DNA repair gene, even though the parents are healthy. A “carrier” means you hold the gene change but may not show symptoms. The genes most often involved are called ERCC6 and ERCC8; they normally help cells fix everyday DNA damage, especially during the process of reading genes. When both copies of one of these genes don’t work, cells can’t keep up with repair, and over time this can affect growth, the brain and nerves, vision and hearing, and sensitivity to sunlight. If both parents are carriers, each pregnancy has a 25% (1 in 4) chance of a child with Cockayne syndrome, a 50% (1 in 2) chance of a carrier child, and a 25% chance of neither. Symptoms and timing can vary widely, even within the same family. Genetic testing for Cockayne syndrome usually looks for changes in ERCC6 and ERCC8, and meeting with a genetic counselor can help you understand results and plan next steps for your family.
Is Cockayne syndrome genetic?
Genetics is central in Cockayne syndrome: it’s caused by inherited changes in DNA repair genes, usually ERCC6 or ERCC8. Most cases follow an autosomal recessive pattern. Variations in these genes influence age at onset, severity, and specific features.
Pharmacogenetics—how genetics influence drug effects
Because Cockayne syndrome stems from changes in genes that help repair DNA, some treatments and medicines need special caution. People with Cockayne syndrome are very sensitive to sunlight, so clinicians try to avoid drugs that raise photosensitivity—such as certain antibiotics, acne medicines, or some pain relievers—or use the lowest effective dose with extra sun protection. Treatments that damage DNA, like high-dose radiation or some chemotherapy drugs, may trigger stronger side effects in Cockayne syndrome, so teams usually look for alternatives or adjust plans carefully. Not every difference in response is genetic, but low body weight, feeding challenges, and kidney or liver function often drive dosing choices in Cockayne syndrome. The Cockayne-related genes themselves are not known to change the main liver enzymes that break down most medicines, so general pharmacogenetic guidance—like testing for how you process some antidepressants, opioids, or seizure medicines—may still be useful on a case-by-case basis. Clinicians individualize therapy and monitor closely for side effects to keep treatment as safe and effective as possible for people living with Cockayne syndrome.
Interactions with other conditions
People living with Cockayne syndrome often find that other health issues can shift the picture day to day, especially infections and feeding problems. A condition may “exacerbate” (make worse) symptoms of another, so a simple cold can increase breathing trouble, raise the risk of aspiration, and make weight loss or dehydration more likely. When Cockayne syndrome occurs together with a related DNA-repair condition called xeroderma pigmentosum (sometimes noted as XP-CS), extreme sun sensitivity and skin damage are common, and the risk of skin cancer rises—something that is uncommon in Cockayne syndrome alone. If cancer is ever diagnosed for unrelated reasons, people with Cockayne syndrome can be unusually sensitive to radiation therapy and certain chemotherapy drugs, so oncologists usually choose gentler, carefully dosed options.
Hearing and vision loss from Cockayne syndrome can compound communication or learning difficulties from other developmental conditions, and early symptoms of Cockayne syndrome may be harder to spot if another diagnosis is already present. Recurrent chest infections, reflux, or dental problems can also interact with swallowing and growth challenges, leading to setbacks that need prompt support. Coordination among specialists—neurology, genetics, ENT, ophthalmology, nutrition, dentistry, and anesthesia—helps tailor treatment plans and reduce medication or procedure risks when multiple conditions are in play.
How genes can cause diseases
Humans have more than 20,000 genes, each carrying out one or a few specific functions in the body. One gene instructs the body to digest lactose from milk, another tells the body how to build strong bones and another prevents the body's cells from beginning to multiply uncontrollably and developing into cancer. As all of these genes combined are the building instructions for our body, a defect in one of these genes can have severe health consequences.
Through decades of genetic research, we know the genetic code of any healthy/functional human gene. We have also identified that in certain positions on a gene, some individuals may have a different genetic letter from the one you have. We call these hotspots "Genetic Variations" or "Variants" in short. In many cases, studies have been able to show that having the genetic letter "G" in the position makes you healthy, but having the letter "A" in the same position disrupts the gene function and causes a disease. Genopedia allows you to view these variants in genes and summarizes all that we know from scientific research, which genetic letters (Genotype) have good or bad consequences on your health or on your traits.
History
Throughout history, people have described children who grew slowly despite eating well, were unusually sensitive to sunlight, and seemed older than their years. Families might recall a toddler who stopped gaining weight, or a school-age child who tired easily after a few minutes outdoors. These everyday observations formed the early picture of what is now known as Cockayne syndrome.
First described in the medical literature as a pattern of growth failure, eye and ear changes, and early aging, the condition was pieced together from careful bedside notes. Early reports focused on the striking mix of short stature, small head size, and sun sensitivity. Over time, descriptions became more complete, noting learning challenges, movement problems, and the way facial features could appear thin or “drawn” as tissues lost fat.
From early theories to modern research, the story of Cockayne syndrome has expanded with new tools. In the mid to late 20th century, laboratory work showed that cells from people with the condition struggled to recover after ultraviolet light exposure. This tied everyday sun sensitivity to a deeper issue in how cells repair day-to-day damage. It also explained why some tissues—skin, eyes, nerves—were affected earlier or more severely than others.
Advances in genetics later identified changes in genes that help with DNA repair after routine stress, which clarified why symptoms accumulate over time. These discoveries also revealed that Cockayne syndrome is not a single, uniform presentation. Some children show early symptoms of Cockayne syndrome in infancy, while others develop features later in childhood. This range helped clinicians recognize milder and more severe forms and avoid missing the diagnosis in children who did not fit the classic picture.
In recent decades, awareness has grown as specialized clinics and family groups shared experiences and data. Careful follow-up across childhood and adolescence showed how hearing, vision, dental health, growth, and movement can change over the years. This long-term view guided practical care—sun protection, nutrition, therapies for hearing and vision—and set expectations for families and care teams.
Looking back helps explain why Cockayne syndrome was once thought to be rare and narrowly defined. Not every early description was complete, yet together they built the foundation of today’s knowledge. With each decade, clearer criteria, confirmatory genetic testing, and coordinated care have improved recognition and support. While research continues, the historical path of Cockayne syndrome shows how bedside observations, lab studies, and family stories can come together to improve everyday life for those living with the condition.