Autosomal dominant Kenny-Caffey syndrome is a rare genetic condition that affects bone growth and mineral balance. People with Autosomal dominant Kenny-Caffey syndrome often have short stature, thickened bones, and small eye openings, and doctors may find low calcium levels. Features usually begin in infancy or early childhood and the condition is lifelong. Many living with Autosomal dominant Kenny-Caffey syndrome do well with regular care, but low calcium can sometimes cause seizures if not treated. Treatment focuses on calcium and vitamin D supplements, eye and dental care, and monitoring growth and development.
Overview
Autosomal dominant kenny-caffey syndromeSymptoms
Autosomal dominant Kenny-Caffey syndrome often appears in infancy or early childhood with proportionate short stature and slow growth. Some infants have low-calcium episodes causing jitteriness, muscle cramps, or seizures. Doctors may also note unusually dense, narrow long bones on imaging.
Outlook and prognosis
Most children with autosomal dominant Kenny-Caffey syndrome grow and learn, but at a slower pace, and need regular follow-up for calcium levels and growth. With early treatment and ongoing monitoring, many attend school and participate in daily activities. Life expectancy is typically near normal when complications are managed.
Causes and risk factors
Autosomal dominant Kenny-Caffey syndrome is caused by pathogenic changes in the FAM111A gene, inherited in an autosomal‑dominant pattern or arising as a new mutation. Risk is highest with an affected parent. No confirmed environmental or lifestyle risk factors are known.
Genetic influences
Genetics are central in autosomal dominant Kenny-Caffey syndrome; a single altered copy of a causative gene can lead to the condition. Most cases arise from variants in FAM111A. Inherited cases carry a 50% chance of passing the variant to each child.
Diagnosis
Doctors suspect Autosomal dominant Kenny-Caffey syndrome from clinical features and growth patterns, then confirm with genetic tests (often FAM111A) and imaging. Blood tests may support the picture. Genetic diagnosis of Autosomal dominant Kenny-Caffey syndrome guides care and family counseling.
Treatment and drugs
Treatment for Autosomal dominant Kenny-Caffey syndrome focuses on steady growth, calcium balance, and eye and bone health. Care often includes vitamin D and calcium, magnesium as needed, growth and thyroid hormone when appropriate, and prompt treatment of low calcium episodes. Regular follow-up with endocrinology, cardiology, eye care, and dentistry helps track changes and support daily life.
Symptoms
Autosomal dominant Kenny-Caffey syndrome (AD‑KCS) tends to show up early with slow, proportionate growth, low-calcium episodes in infancy, and a soft spot on the head that stays open longer. These features can touch day-to-day life in the early years, then often settle into a pattern of shorter adult height and routine monitoring. Features vary from person to person and can change over time. Parents may first notice early features of autosomal dominant Kenny-Caffey syndrome, like jitteriness from low calcium or a larger soft spot.
Growth is slower than peers and body proportions are balanced. Many living with autosomal dominant Kenny-Caffey syndrome reach a shorter adult height and benefit from regular growth checks.
Low calcium (hypocalcemia) in infancy can cause jitteriness, muscle cramps, tingling around the mouth, or seizures. It stems from low parathyroid hormone levels and is usually managed with calcium and vitamin D.
The soft spot (fontanelle) on the head may stay open longer than usual. Pediatricians watch head growth over time and advise simple precautions without major activity limits.
X-rays often show thicker outer bone and a narrow marrow space in the long bones. This isn’t usually felt day to day, but it helps clinicians confirm Kenny-Caffey syndrome.
How people usually first notice Autosomal dominant kenny-caffey syndrome?
Many families first notice something is different when a newborn with autosomal dominant Kenny-Caffey syndrome is smaller than expected and has trouble feeding or seems unusually tired, prompting early pediatric checkups. Doctors may pick up the first signs of autosomal dominant Kenny-Caffey syndrome through low calcium levels causing jitteriness or muscle cramps, sometimes with seizures, along with short stature and distinctive facial or bone features on exam or X‑rays. For some, how autosomal dominant Kenny-Caffey syndrome is first noticed is during routine newborn screening or the first weeks of life when growth doesn’t follow the usual curve and blood tests reveal electrolyte imbalances.
Types of Autosomal dominant kenny-caffey syndrome
Autosomal dominant Kenny-Caffey syndrome has more than one recognized clinical variant, shaped by the specific gene involved. These variants share a core picture of short stature and bone changes, but day-to-day features like calcium levels, vision, and learning support needs can differ. Symptoms don’t always look the same for everyone. Knowing the types of Autosomal dominant kenny-caffey syndrome can help you understand why two people in the same family might have different challenges.
Type 2 (FAM111A)
This classic autosomal dominant form often includes short stature, thickened long bones, and small eye openings. Low calcium from underactive parathyroid glands can cause muscle cramps or tingling, especially in infancy. Eye and dental differences are reported in some people.
Craniofacial form
Some families have more noticeable facial features with smaller eye openings and a narrow forehead. Calcium problems may be milder or vary over time. Learning differences can range from none to mild.
Milder familial variant
In certain families, height and bone changes are present but day-to-day symptoms are subtler. People may have few or no calcium-related episodes after early childhood. Routine checks of growth, calcium, and vision still matter for types of Autosomal dominant kenny-caffey syndrome.
What genetics can tell you about symptoms
People with autosomal dominant Kenny-Caffey syndrome often have short stature, small or absent bones in the skull’s soft spots, and low calcium symptoms like muscle cramps or tingling, which stem from variants in the FAM111A gene affecting bone growth and parathyroid function. Some also show thickened bones, small eye openings, or delayed tooth eruption because the same gene changes disrupt how bones remodel and how calcium is regulated.
Causes and risk factors
Autosomal dominant Kenny-Caffey syndrome is usually caused by a change in the FAM111A gene. It follows an autosomal dominant pattern, so an affected parent has a 50% chance to pass it to each child. The main risk factors for autosomal dominant Kenny-Caffey syndrome are having an affected parent or carrying the FAM111A change. Many cases arise as a new gene change, so there may be no family history. Genes set the stage, but environment and lifestyle often decide how the story unfolds.
Environmental and biological risk factors
If you’re planning a pregnancy or already expecting, it’s natural to wonder what might raise or lower the chance of Autosomal dominant kenny-caffey syndrome. Being exposed to risks in your body or environment doesn’t mean illness is inevitable. Most cases appear without a clear outside trigger, and risk factors don’t predict the exact course or early symptoms of Autosomal dominant kenny-caffey syndrome. Here are the main biological and environmental points researchers consider today.
Conception with an older father is linked to a higher chance of rare, new conditions that begin during embryo development. This pattern has been seen across several rare conditions present from birth and may be relevant to Autosomal dominant kenny-caffey syndrome. Plenty of people with similar exposures live without developing the condition.
Older maternal age is a general risk for some conditions present from birth, though its role in Autosomal dominant kenny-caffey syndrome is unclear. If there is any effect, it appears smaller than the impact of the father’s age.
No specific pregnancy or home exposures have been proven to raise the chance of Autosomal dominant kenny-caffey syndrome. Research to date has not linked infections, air pollution, heavy metals, or common household chemicals to higher risk. Doctors typically focus on routine prenatal care rather than avoiding one particular exposure.
Genetic risk factors
The genetic picture centers on one gene called FAM111A. In autosomal dominant Kenny-Caffey syndrome, disease-causing changes in this gene are either inherited from a parent or occur for the first time in a child. People with the same risk factor can have very different experiences. Genetic testing can clarify the genetic causes of autosomal dominant Kenny-Caffey syndrome by pinpointing the exact FAM111A change in a family.
FAM111A gene variants: Most cases trace to changes in a single gene, FAM111A. These gene changes disrupt normal development and lead to the features seen in autosomal dominant Kenny-Caffey syndrome.
Dominant inheritance: If a parent carries the FAM111A variant, each child has a 50% chance of inheriting it. An inherited variant can lead to autosomal dominant Kenny-Caffey syndrome, although symptoms can differ in the same family.
De novo variants: Many people are the first in their family with the condition because the FAM111A change happened for the first time in that egg or sperm. In these families, the chance that future children are affected is usually low but not zero.
Parental mosaicism: Rarely, an unaffected parent carries the FAM111A change in a small fraction of their egg or sperm cells (germline mosaicism). This can raise the recurrence risk above the general population, even when parents test negative in blood.
Family history: Having a parent or close relative with a confirmed FAM111A variant is the strongest genetic risk factor for autosomal dominant Kenny-Caffey syndrome. Knowing the exact familial variant allows targeted testing of relatives.
Variant effects: Different changes in FAM111A can have different effects on the body. This helps explain why features and severity vary among people living with this condition.
Lifestyle risk factors
This condition is genetic and not caused by lifestyle choices, but daily habits can meaningfully influence symptoms, complications, and quality of life. In particular, calcium balance, bone health, and seizure risk can shift with diet, activity, and routines. Put simply, while lifestyle risk factors for Autosomal dominant kenny-caffey syndrome do not create the disorder, they can make symptoms easier or harder to manage.
Regular intake as prescribed supports steadier calcium levels and reduces tingling, cramps, and seizure risk. Skipping supplements or low-calcium diets can trigger hypocalcemia symptoms.
Cola and other high-phosphate drinks bind calcium and can worsen low calcium levels. Limiting them helps stabilize calcium and reduces neuromuscular irritability.
High caffeine or salty foods increase urinary calcium loss. Cutting back can help maintain serum calcium and reduce cramp or tetany episodes.
Consistent use of calcium and active vitamin D (if prescribed) keeps levels stable. Irregular dosing increases swings in calcium and raises risk of symptoms and ER visits.
Risk prevention
Autosomal dominant Kenny-Caffey syndrome is inherited, so you can’t prevent the condition itself. The focus is lowering the chance of complications—especially low calcium episodes, growth concerns, and bone problems—through steady monitoring and early care. Even if you can’t remove all risks, prevention can reduce their impact. Planning for pregnancy and newborn screening in families with this condition may help catch issues early.
A genetics visit can explain inheritance, chances for future children, and testing options. This can include carrier testing for family members and discussion of IVF with embryo testing or prenatal testing.
For babies at risk, early blood tests can catch low calcium before symptoms start. Treating low calcium promptly may prevent seizures or heart rhythm problems.
Regular monitoring and tailored supplements can help keep calcium in a safe range. Your care team may also track magnesium and parathyroid hormone, which influence calcium stability.
Illness, poor intake, or dehydration can trigger drops in calcium. A written plan for fluids, nutrition, and when to get labs can reduce emergency visits.
Transmission
Autosomal dominant kenny-caffey syndrome is not infectious—you can’t catch it from someone and it doesn’t spread through contact. The genetic transmission of Autosomal dominant kenny-caffey syndrome follows an autosomal dominant pattern: when a parent has the condition, each pregnancy has a 50% chance that the child will inherit it.
Sometimes it appears for the first time in a child because of a new genetic change, even when both parents are unaffected. Genetic counseling can help explain how Autosomal dominant kenny-caffey syndrome is inherited in your family and discuss testing options for parents, pregnancies, or siblings.
When to test your genes
Consider genetic testing if you have features of autosomal dominant Kenny‑Caffey syndrome (short stature, thickened bones with small marrow cavities, calcium problems) or a close relative with a confirmed diagnosis. Test preconception or during pregnancy for family planning. If already diagnosed, testing guides calcium/vitamin D management and screens relatives who may be mildly affected.
Diagnosis
Autosomal dominant Kenny-Caffey syndrome is usually identified by a mix of recognizable features and confirmed with targeted tests. Because it’s rare, doctors often piece together the pattern from growth history, exam findings, and imaging before ordering a gene test. Early and accurate diagnosis can help you plan ahead with confidence. The genetic diagnosis of autosomal dominant Kenny-Caffey syndrome is typically confirmed with a DNA test once the clinical picture fits.
Doctors look for proportionate short stature, delayed closure of the soft spot on the head, and small hands and feet. Facial features may include a broad forehead, and head size can be larger than expected. These clues guide which tests come next.
Providers track height, weight, and head size over time to see a consistent pattern. For many, growth slows after birth while development is otherwise typical. This timeline helps separate it from other growth conditions.
Blood tests may check calcium, phosphate, magnesium, and parathyroid hormone levels. Some people—especially in infancy—may have low calcium due to low parathyroid hormone. Results help support the diagnosis and rule out other causes of low calcium.
Imaging of the long bones can show thickened outer bone with a narrowed inner canal, a hallmark pattern in this condition. Skull and hand films may show additional changes that fit the syndrome. These imaging findings help distinguish it from look-alike disorders.
Stages of Autosomal dominant kenny-caffey syndrome
Autosomal dominant kenny-caffey syndrome does not have defined progression stages. It’s a lifelong genetic condition in which features like shorter height and characteristic bone findings usually appear early and stay fairly steady, while low calcium episodes may flare in infancy or childhood and then improve. People may notice early symptoms of autosomal dominant kenny-caffey syndrome such as jitteriness, muscle cramps, or seizures from low calcium in babies, and slower growth over time. Different tests may be suggested to help confirm what’s going on, including blood tests for calcium and related hormones, X-rays to look at bone structure, and sometimes genetic testing; ongoing care often includes regular checks of growth, vision, teeth, and calcium levels.
Outlook and prognosis
Daily routines often adapt as people with autosomal dominant Kenny-Caffey syndrome (ADKCS) grow and gain strength—think extra time for feeding in infancy, more frequent dental checks, and regular vision appointments. The outlook is not the same for everyone, but many children catch up in motor skills and height to some degree, especially with nutrition and hormone guidance. Serious complications are uncommon in the dominant form; life expectancy is generally near typical when calcium levels are well managed and infections are treated promptly.
Here’s what research and experience suggest about the future. Some people experience early symptoms of autosomal dominant Kenny-Caffey syndrome like low calcium with muscle cramps or seizures, while others have milder signs such as small stature and dental or vision differences. With ongoing care, many people maintain good overall health, attend school, work, and lead active lives. Mortality is considered low in ADKCS; most risks relate to untreated low calcium or rare infections, which can be mitigated with early recognition and routine care.
Understanding the prognosis can guide planning and everyday choices. Regular follow-up for growth, calcium and vitamin D balance, thyroid function, and vision can prevent setbacks and support steady progress into adulthood. Talk with your doctor about what your personal outlook might look like, including how genetics, lab trends, and response to supplements shape your long-term plan.
Long-term effects
Autosomal dominant Kenny-Caffey syndrome tends to have a stable outlook, with many people living full lives and typical learning. Long-term effects vary widely, and not everyone has the same set of features or the same degree of change. Short stature and certain bone traits usually persist into adulthood. Although people sometimes search for “early symptoms of autosomal dominant Kenny-Caffey syndrome,” doctors focus more on the lasting features that shape day-to-day life over time.
Height often tracks below average from childhood onward. Adult height is typically shorter than peers. Growth patterns are generally steady rather than falling off suddenly.
Long bones can develop thicker outer walls with narrowed inner canals. This pattern may contribute to limb aches or fatigue after activity. Fractures are not common but can occur.
Soft spots on the skull may close later than usual in childhood. Head shape and facial proportions can look mildly different but tend to be stable over time.
Some experience low calcium levels early in life, which often improves with age. Later on, calcium levels are usually steady, though stress or illness can occasionally unmask dips.
How is it to live with Autosomal dominant kenny-caffey syndrome?
Living with autosomal dominant Kenny-Caffey syndrome often means shorter stature, small bones, and low calcium levels that can trigger muscle cramps, tingling, or occasional seizures, especially during illness or stress. Daily life usually involves routine calcium and vitamin D supplementation, periodic lab checks, eye and dental care, and planning around fatigue or muscle symptoms, yet many people can attend school, work, and family activities with reasonable accommodations. For loved ones, the biggest roles are watching for early signs of low calcium, supporting medical appointments, and encouraging a balanced routine that includes rest, nutrition, and exercise as advised. With consistent monitoring and a responsive care plan, most families find a steady rhythm that keeps health stable and goals within reach.
Treatment and drugs
Treatment for autosomal dominant Kenny-Caffey syndrome focuses on easing symptoms and supporting growth, bone health, and vision over time. Care often includes calcium and active vitamin D to manage low calcium levels, magnesium if needed, and careful monitoring to prevent both cramps and kidney stone risk; a doctor may adjust your dose to balance benefits and side effects. Many people also benefit from growth and bone support such as nutrition counseling, treatment of low phosphate if present, and, in some cases, growth hormone after an endocrine evaluation. Regular eye care for corneal or optic nerve issues, dental care for enamel problems, and physical or occupational therapy can help with day-to-day function and comfort. Treatment plans often combine several approaches, with follow-up visits to track labs, growth, and bone strength and to fine-tune care as needs change.
Non-drug treatment
Non-drug care for Autosomal dominant kenny-caffey syndrome focuses on strengthening bones, supporting growth and development, and making daily life easier. Alongside medicines, non-drug therapies can help manage motor skills, learning needs, hearing or vision issues, and dental concerns. Spotting early symptoms of Autosomal dominant kenny-caffey syndrome can guide which therapies to start first. Care plans are individualized and usually involve a coordinated team over time.
Targeted exercises build strength, balance, and coordination. This can reduce falls and support safe movement at school or work. Programs are adjusted as children grow or as adult needs change.
Skills for dressing, handwriting, and daily tasks are practiced in small steps. Therapists can suggest adaptive tools to make tasks easier and prevent fatigue. Family members often play a role in supporting new routines.
Therapy can address articulation, language, and oral-motor coordination for clearer speech and safer chewing. Strategies may include pacing, breath control, and communication supports. Early referral often improves school participation.
A dietitian helps plan calcium- and protein-rich meals to support bones and growth. Guidance may include vitamin D–rich foods and practical meal planning. Keep track of how lifestyle changes affect your symptoms.
Your genes may have an impact on how drugs work for you
Genes can change how your body processes certain medicines for autosomal dominant Kenny-Caffey syndrome, affecting dose needs, benefits, and side effects. Pharmacogenetic testing, when available, can guide safer choices for calcium, vitamin D, and symptom‑targeting treatments.
Pharmacological treatments
Treatment focuses on keeping calcium in a safe range and preventing symptoms like muscle cramps, tingling, or seizures. For Autosomal dominant kenny-caffey syndrome, doctors often use vitamin D–based medicines and minerals, adjusting them over time to match the body’s needs. Not everyone responds to the same medication in the same way. This approach helps protect growth, bones, and nerves, even when early symptoms of Autosomal dominant kenny-caffey syndrome are easy to miss.
Calcitriol (active vitamin D) helps the gut absorb calcium when natural parathyroid hormone is low. It is taken by mouth and adjusted based on blood and urine tests to avoid too-high calcium. Doses are changed gradually as needs shift.
Calcium carbonate or citrate can raise blood calcium and ease tingling, cramps, or fatigue. Taking it with meals improves absorption, and routine labs help prevent over-supplementation.
Low magnesium can block calcium from normalizing. Short courses of oral or IV magnesium are used if tests show a deficit.
If urine calcium runs high while on calcium and vitamin D, a thiazide (such as hydrochlorothiazide) can reduce kidney calcium loss. This helps protect the kidneys and may allow lower calcium doses.
Genetic influences
Autosomal dominant Kenny-Caffey syndrome usually stems from a change in a single gene called FAM111A. Because it’s autosomal dominant, one altered copy is enough to cause the condition, and a parent living with it has a 50% chance (1 in 2) of passing it to each child. Many people, however, are the first in their family with the condition because the gene change happened for the first time at conception (often called a de novo variant). FAM111A is involved in bone development and the body’s handling of minerals like calcium; depending on where and how the gene is altered, features and severity can differ from one person to the next. DNA testing can sometimes identify these changes. Confirming the genetic cause can guide care, clarify the chance of recurrence in a future pregnancy, and explain why early symptoms of autosomal dominant Kenny-Caffey syndrome may vary among siblings. Genetic counseling is often recommended to discuss testing options for parents and relatives and to interpret results in the context of family plans.
Is Autosomal dominant kenny-caffey syndrome genetic?
Genetics are central in autosomal dominant Kenny-Caffey syndrome; a single altered copy of a causative gene can lead to the condition. Most cases arise from variants in FAM111A. Inherited cases carry a 50% chance of passing the variant to each child.
Pharmacogenetics—how genetics influence drug effects
In autosomal dominant kenny-caffey syndrome, the gene change lowers parathyroid hormone signals, so treatment centers on keeping calcium steady with supplements and the active form of vitamin D (calcitriol). Regular vitamin D tablets often aren’t enough, so doctors tailor calcitriol and calcium doses to lab results and day-to-day symptoms, adjusting over time to avoid both low calcium and calcium buildup in urine or kidneys. Some medicines—such as certain anti-seizure drugs or steroids—can interfere with vitamin D or calcium balance, so your care team will check for interactions and may change doses. Genetic testing can sometimes identify how your body handles certain medicines, but for autosomal dominant kenny-caffey syndrome it mainly confirms the diagnosis and helps plan monitoring rather than picking a specific drug. The gene change that causes this condition isn’t known to alter how your liver processes most common drugs, so usual pharmacogenetic advice for other prescriptions is the same as in the general population. If other health issues call for medicines with known gene–drug guidance, that testing would be considered separately, while the core treatment for autosomal dominant kenny-caffey syndrome remains guided by calcium levels, symptoms, and safety checks.
Interactions with other conditions
Illnesses and treatments that disturb calcium balance tend to hit harder for people living with autosomal dominant Kenny-Caffey syndrome. A condition may “exacerbate” (make worse) symptoms of another, so infections, stomach bugs, or surgery can tip calcium levels lower and bring on muscle cramps, tingling, or even seizures. Kidney disease, low vitamin D, poor magnesium levels, or gut conditions that affect absorption can make calcium control more difficult, and some medicines—like loop diuretics, long-term steroids, or certain anti-seizure drugs—can also lower calcium or vitamin D. Because low calcium can provoke seizures or lengthen the heart’s QT interval, those with epilepsy, known heart rhythm problems, or medicines that affect heart rhythm may need closer monitoring and coordinated care. If osteoporosis is also present, treatments such as bisphosphonates can briefly lower blood calcium, so doctors usually plan extra lab checks and adjust calcium and vitamin D. Intercurrent infections sometimes unmask early symptoms of autosomal dominant Kenny-Caffey syndrome by stressing the body’s calcium balance, and related genetic diagnoses in the same family may share overlapping bone and calcium features.
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
Families and communities once noticed patterns of short stature and small, strong bones appearing in several relatives, often across generations. In everyday life, this meant a child who stayed much smaller than classmates yet kept up in school and play, sometimes with frequent checks for low calcium. Doctors took note of the combination of short height, dense bones on X‑rays, and episodes of muscle cramping or tingling from low calcium, and began to group these features together.
First described in the medical literature as a distinctive form of short stature with thickened bones and low calcium, the condition later took on the name Autosomal dominant Kenny-Caffey syndrome as more families were reported. Early case reports focused on outward features and X‑ray findings. Over time, descriptions became more precise, separating this autosomal dominant form from a different, more severe autosomal recessive type that can include eye and immune problems. This helped clinicians recognize that not all “Kenny-Caffey” diagnoses meant the same outlook or care needs.
Advances in genetics confirmed what families had long observed: the autosomal dominant pattern, where an affected parent can pass the condition to a child with a 50% chance in each pregnancy. In recent decades, awareness has grown as clinicians linked the syndrome to changes in a gene that acts a bit like a dimmer switch for bone growth and calcium balance. This shift—from pattern recognition to a gene-based diagnosis—made it possible to provide clearer counseling, support targeted testing, and avoid confusion with other causes of short stature and low calcium.
From early theories to modern research, the story of Autosomal dominant Kenny-Caffey syndrome shows how careful observation, family histories, and genetics fit together. Not every early description was complete, yet together they built the foundation of today’s knowledge. Now, many living with the syndrome are identified earlier, sometimes in childhood when low calcium first appears, and can receive straightforward treatments like calcium and vitamin D along with routine growth monitoring. Knowing the condition’s history helps explain why doctors ask about relatives’ height, childhood lab results, and X‑rays—clues that guided the past and still improve care today.