Fish-eye disease is a rare genetic eye condition that causes clouding of the corneas. People with fish-eye disease often notice blurry vision, glare, and trouble seeing at night, while eye exams show corneal haze. It is lifelong and usually recognized in childhood or early adulthood. Vision changes can be mild to moderate and do not affect life expectancy. Treatment focuses on eye drops for comfort, glasses or contacts for clarity, and in advanced cases corneal transplant to improve vision.
Overview
Fish-eye diseaseSymptoms
Fish-eye disease mainly causes painless, gradual clouding of the corneas, leading to blurry vision and glare or light sensitivity. Early signs of fish-eye disease often appear in childhood or teens and include hazy eyes without redness.
Outlook and prognosis
Most people with fish-eye disease develop slowly progressive clouding of the corneas, leading to blurry vision and glare that can affect driving or night reading. With regular eye care, lubricating drops, tinted lenses, and, if needed, corneal transplant, many maintain useful vision. Lifespan and general health are typically unaffected.
Causes and risk factors
Fish-eye disease results from inherited LCAT gene changes causing partial enzyme deficiency (autosomal recessive). Risk is highest with two carrier parents or parental consanguinity; family history matters. Diet, smoking, and other lipid-raising factors can intensify low HDL features.
Genetic influences
Genetics are central in Fish-eye disease. It’s caused by inherited changes in the LCAT gene, usually passed in an autosomal recessive pattern. Variations determine enzyme activity, severity, and family risk; carrier and diagnostic genetic testing can clarify inheritance and guide counseling.
Diagnosis
Doctors suspect Fish-eye disease when corneal clouding and very low HDL cholesterol appear. Diagnosis is supported by slit-lamp exam, lipid testing, and reduced LCAT enzyme activity. Genetic diagnosis of Fish-eye disease uses LCAT gene testing to confirm.
Treatment and drugs
Treatment for Fish-eye disease focuses on easing symptoms and protecting vision. Doctors may use eye lubricants, omega‑3 supplements, and lipid‑lowering medicines like statins or PCSK9 inhibitors; some consider lipid apheresis in selected cases. Regular eye exams help manage corneal clouding and glare.
Symptoms
Fish-eye disease mainly affects the eyes, leading to cloudy corneas and vision that can look hazy or glare-prone. People often notice early features of Fish-eye disease in childhood or the teen years, though some learn about it later during an eye exam. In everyday life, bright light may feel harsh, and night driving can be harder due to halos. Features vary from person to person and can change over time.
Vision may look foggy or blurred across the whole field. You might notice small changes at first, like wiping your lenses more often even when they’re clean. In Fish-eye disease, glasses may sharpen letters but not remove the general haze.
Bright light can feel uncomfortable and cause squinting or tearing. Glare from sunlight or screens may be intense, making outdoor activities or computer work tiring. Sunglasses with good UV protection often help.
Halos or starbursts around headlights are common. Driving at night can feel more stressful because of glare from oncoming traffic. Choosing well-lit routes or avoiding nighttime driving may be helpful.
Eye specialists can see a gray-white cloudiness across the cornea on exam. Clinicians call this corneal opacity, which means the normally clear front window of the eye looks hazy. The surface itself usually isn’t painful.
How people usually first notice Fish-eye disease?
People often first notice fish-eye disease through very cloudy, hazy corneas that make the eyes look milky and cause blurred vision or glare, especially in bright light. This condition, a rare inherited form of partial LCAT deficiency, is usually picked up in childhood or early adulthood when persistent vision problems lead to an eye exam showing markedly low HDL (“good”) cholesterol and corneal opacities. For many, the first signs of fish-eye disease are trouble seeing clearly at night or halos around lights, prompting a visit to an eye doctor who recognizes how fish-eye disease is first noticed.
Types of Fish-eye disease
Fish-eye disease is a genetic condition linked to low activity of an enzyme that helps process certain fats in the body. It is considered a milder, partial form of a broader enzyme deficiency, so most discussions of variants focus on where it sits on that spectrum. Clinicians often describe them in these categories: a severe, full enzyme deficiency and this milder, partial deficiency. If you’re comparing types of Fish-eye disease, it’s helpful to know it is typically viewed as a subtype rather than having multiple distinct variants of its own.
Fish-eye subtype
This partial enzyme deficiency leads mainly to very low HDL cholesterol and cloudy corneas that can blur vision over time. Other organs are usually spared, and symptoms often stay focused on the eyes and lipid levels.
Classic severe form
In the full enzyme deficiency, problems often extend beyond the eyes, with nerve, kidney, and other organ involvement. This more widespread pattern is not considered Fish-eye disease but sits on the same enzyme spectrum.
What genetics can tell you about symptoms
Fish-eye disease, caused by changes in the LCAT gene, leads to very low HDL cholesterol and cloudy corneas that blur vision or cause glare. Some also develop eye irritation and early corneal opacity, while most do not have liver or kidney problems.
Causes and risk factors
Fish-eye disease happens when a change in the LCAT gene lowers this enzyme’s function. A child is affected only if both parents carry and pass on the same nonworking gene. Some risks are written in our DNA, passed down through families. Risk is higher with a family history or when parents are related, but lifestyle or environment do not cause Fish-eye disease. Healthy habits can support cholesterol and overall health, and relatives may seek genetic counseling or watch for early symptoms of Fish-eye disease.
Environmental and biological risk factors
Fish-eye disease is present from birth and primarily arises from internal biological changes, so environmental risk factors for Fish-eye disease are limited. Some risks are carried inside the body, others come from the world around us. Below are biological and environmental exposures that could slightly increase the chance of a new change at conception. For most families, these influences are uncommon and the absolute risk remains low.
As fathers get older, new DNA changes in sperm become more frequent. This can slightly raise the chance of rare single-gene conditions at conception, including Fish-eye disease.
Significant radiation to the testes or ovaries before conception can damage DNA in reproductive cells. This may modestly raise the chance of a new, random change when pregnancy begins.
Some chemotherapy medicines and pelvic or testicular/ovarian radiation can injure sperm or eggs. For Fish-eye disease, this would matter only if a new change arose at conception, which remains uncommon.
Older maternal age mainly increases risks of chromosome conditions rather than single-gene changes. It is not considered a major driver for Fish-eye disease.
Genetic risk factors
Genetically, Fish-eye disease most often stems from changes in the LCAT gene, which helps your body package cholesterol for transport. The condition follows an autosomal recessive pattern, so you typically need two altered copies to develop it. In some cases, genetic testing can give a clearer picture of your personal risk. Key genetic risk factors for Fish-eye disease include having two carrier parents or certain family patterns.
LCAT gene changes: Fish-eye disease results from changes in the LCAT gene, which helps package cholesterol for transport. These changes reduce the enzyme’s activity mainly on HDL (good cholesterol), leading to low HDL levels and corneal clouding. Different variants can affect the enzyme to different degrees.
Autosomal recessive: The condition is inherited in an autosomal recessive way. You usually need two altered LCAT copies—one from each parent—to develop Fish-eye disease. Parents with one altered copy are typically healthy.
Two carrier parents: When both parents carry an LCAT change, each child has a 25% chance to have Fish-eye disease. There is also a 50% chance the child will be a carrier like the parents and a 25% chance to inherit no changes. This risk repeats with each pregnancy.
Carrier state: Carriers have one altered and one typical LCAT gene. They usually have no symptoms but may show low HDL on a lipid test. Knowing carrier status can guide family planning.
Family history: Having an affected sibling or close relative raises the chance that others in the family are carriers. If both parents are carriers, siblings have a higher chance to be affected. Targeted testing in relatives can clarify risks.
Consanguinity: When parents are related by blood, they are more likely to share the same rare LCAT variant. This increases the likelihood their children inherit two altered copies.
Variant type matters: Changes that mainly reduce LCAT’s action on HDL cause Fish-eye disease, sometimes called alpha-LCAT deficiency. Other, more severe LCAT changes can cause a different condition with kidney problems. The exact variant can help predict features and timing.
Compound heterozygous: Fish-eye disease can occur when two different LCAT changes are present, one on each copy of the gene. This can function like having two of the same change. Severity can vary with the combination.
Founder effect: In some families or regions, a single older LCAT variant has been passed down through generations. This can raise the local carrier rate and the chance two carriers meet. Overall prevalence is still very low.
Variable expression: Most with two disease-causing LCAT changes develop corneal clouding, but the age of onset and lab findings can differ. This variability often relates to the specific variants involved.
Lifestyle risk factors
Fish-eye disease is inherited and not caused by lifestyle, but daily habits can influence symptom burden and long-term complications. In particular, choices that affect triglycerides, LDL, inflammation, and vascular health can matter when HDL function is already impaired. This overview focuses on how lifestyle affects Fish-eye disease and highlights the lifestyle risk factors for Fish-eye disease. Work with your care team to tailor these strategies to your lipid profile and vision needs.
Diets high in saturated and trans fats raise LDL and triglycerides, increasing atherosclerosis risk when HDL is already ineffective. Reducing these fats can lessen cardiovascular strain even though HDL levels remain low.
Rapidly absorbed sugars and starches elevate triglycerides and remnant lipoproteins that worsen dyslipidemia in Fish-eye disease. Limiting them can improve post-meal lipids and reduce vascular risk.
Lack of regular aerobic activity increases triglycerides and impairs endothelial function, compounding risk in the setting of very low HDL. Consistent exercise can lower triglycerides and improve vascular health despite not fixing the LCAT defect.
Tobacco use further damages HDL function and oxidizes LDL, accelerating plaque formation when protective HDL is deficient. Quitting reduces inflammation and slows atherosclerosis progression in Fish-eye disease.
Risk prevention
Fish-eye disease is a genetic condition you can’t fully prevent, but you can lower the chance of complications affecting the eyes and heart. Prevention is about lowering risk, not eliminating it completely. Regular eye care and heart-healthy habits help protect vision and reduce cardiovascular risk. Acting early when early symptoms of fish-eye disease appear—like glare or blurry vision—can also limit day-to-day impact.
Routine checks with an eye specialist can track corneal clouding and catch changes early. This helps guide treatments to reduce glare, dryness, and vision strain in fish-eye disease.
Wearing UV-blocking sunglasses and lenses with anti-glare coating can reduce light sensitivity from corneal haze. This can make driving and screen time more comfortable.
People with fish-eye disease can have very low HDL and higher heart risk. Regular checks of cholesterol, blood pressure, and blood sugar help tailor prevention plans.
Choose a diet lower in saturated fat and trans fat, with more fiber from plants and fish rich in omega-3s. This supports cholesterol control when HDL is low.
Transmission
Fish-eye disease is not contagious. You can’t catch it from someone through touch, coughing, sharing utensils, or blood contact; it isn’t spread between people.
Fish-eye disease is inherited in an autosomal recessive pattern. This means if both parents carry one changed copy of the gene, each pregnancy has a 25% (1 in 4) chance of a child with the disease, a 50% (1 in 2) chance of a child who is a carrier, and a 25% (1 in 4) chance of a child with no changed copies. Most cases reflect genetic transmission of Fish-eye disease from carrier parents; new gene changes can happen but are uncommon.
When to test your genes
Test your genes if you have very high HDL cholesterol that’s unusually low in function, corneal clouding causing blurry vision, or a close relative with Fish‑eye disease (LYCAT/LCAT deficiency). Early testing helps tailor monitoring, eye care, and heart‑risk prevention. Consider testing before pregnancy for family planning.
Diagnosis
For many, the first step comes when everyday activities start feeling harder—like night driving due to glare or hazy vision—prompting an eye check. An eye specialist often spots telltale corneal clouding, and blood tests then look at cholesterol patterns. Many people feel relief just knowing what’s really going on. From there, doctors confirm findings with enzyme and genetic tests to be sure this is Fish-eye disease and not a related condition.
An ophthalmologist examines the front of the eye with a slit-lamp to look for diffuse corneal clouding typical of Fish-eye disease. These findings can explain glare and blurred vision and help separate it from more common causes of cloudy corneas.
A standard blood test often shows very low HDL (“good”) cholesterol in people with Fish-eye disease. Total cholesterol and triglycerides may be normal or only mildly changed, which can be a helpful clue.
A specialized lab test measures the activity of the LCAT enzyme in blood. In Fish-eye disease, activity is partially reduced, especially the part that works with HDL, which supports the diagnosis.
Testing the LCAT gene can confirm the genetic diagnosis of Fish-eye disease by identifying the underlying change. This also helps guide testing for at-risk relatives and supports accurate counseling.
Stages of Fish-eye disease
Fish-eye disease does not have defined progression stages. It’s a lifelong genetic condition where corneal clouding and very low HDL can develop at different speeds, so early symptoms of Fish-eye disease don’t line up neatly into set stages. Different tests may be suggested to help confirm the diagnosis and check for related issues over time. These often include an eye exam with a slit lamp to look for corneal haze, a fasting lipid panel to measure HDL, and, in some cases, genetic testing for changes in the LCAT gene.
Outlook and prognosis
Thinking about the years ahead with Fish-eye disease, most people focus on how vision may change and what can be done to protect it. Many notice hazy or glare-prone vision, especially at night, that slowly progresses; driving at dusk, reading street signs, or seeing in bright sunlight can become tougher over time. Doctors call this the prognosis—a medical word for likely outcomes. Fish-eye disease mainly affects the corneas and does not typically shorten life expectancy; it’s considered an eye-limited condition rather than a whole‑body illness.
Over time, most people maintain useful vision for many daily tasks, though some eventually need stronger lenses, tinted filters, or specialized contacts. Corneal transplants or procedures like superficial keratectomy may be considered if clouding becomes severe; these can improve clarity but may need repeat care years later. Genetic testing can sometimes provide more insight into prognosis, especially to distinguish Fish-eye disease from related LCAT disorders that do affect other organs. Knowing the early symptoms of Fish-eye disease—such as increased light sensitivity, halos around lights, or worsening night vision—can help you and your eye team plan timely steps.
With ongoing care, many people maintain independence, work, and driving, though night driving may remain limited. Severe vision loss is uncommon, but not impossible; if it occurs, low‑vision tools and orientation training can keep daily life manageable. Talk with your doctor about what your personal outlook might look like, including how often to check your corneas and when to consider procedures. Understanding the prognosis can guide planning and make room for practical adjustments that protect vision and quality of life.
Long-term effects
For many living with Fish-eye disease, the day-to-day impact shows up most in how the eyes handle light, glare, and sharp focus. Many remember early symptoms of Fish-eye disease as glare and halos, but over time the lasting features center on the eyes and cholesterol profile. Long-term effects vary widely. Most people do not lose total vision, but clarity can be reduced, and doctors may also keep an eye on heart health over the years.
A gradual, milky haze builds up in the clear front window of the eye. It often progresses slowly and can plateau. Severe vision loss is uncommon.
Distance and night vision may be less sharp, and halos around lights are common. Reading fine print or driving at night can feel harder over time.
Bright light and glare can feel harsh, especially outdoors or with oncoming headlights. People may notice squinting and eye fatigue in these settings.
Blood tests typically show persistently low HDL cholesterol. Other cholesterol numbers can be closer to typical ranges, depending on the individual.
How is it to live with Fish-eye disease?
Living with Fish-eye disease, a rare inherited lipid disorder, often means coping with very blurry vision from early life due to cloudy corneas, while the rest of the body usually feels well. Daily life can involve glare sensitivity, trouble seeing at night, and needing frequent eye care, protective sunglasses, and visual aids to manage school, work, and driving decisions. People around you may need to adjust lighting, offer rides after dark, and understand that eye discomfort or squinting isn’t rudeness but a feature of the condition. Many find that planning ahead, regular ophthalmology visits, and clear communication with family, teachers, and employers make day-to-day activities more manageable and safe.
Treatment and drugs
Treatment for Fish-eye disease focuses on easing symptoms and protecting the eyes over time. Because this condition reduces certain blood fats and leads to corneal clouding, doctors often start with eye-focused care such as lubricating drops for comfort, tinted or anti-glare lenses for light sensitivity, and regular eye exams to track changes; some people benefit from specialty contact lenses to improve contrast and clarity. If corneal haze becomes severe and vision drops significantly, a corneal transplant may be considered, while still understanding the underlying metabolic issue continues. Alongside medical treatment, lifestyle choices play a role, including protecting eyes from UV light with sunglasses, managing cardiovascular risks with a heart-healthy diet and exercise, and avoiding smoking. Ask your doctor about the best starting point for you, and how often you should check your vision and lipid levels so the plan can be adjusted as your needs change.
Non-drug treatment
Fish-eye disease can blur vision and make bright light feel harsh in day-to-day life. Non-drug treatments often lay the foundation for comfort, safety, and maintaining independence. The right mix usually includes eye-specific strategies, practical vision aids, and healthy routines for heart health. Care plans are individualized and may change as vision changes over time.
Tinted sunglasses and anti-glare lenses can cut glare and ease light sensitivity. Consistent eye protection may make outdoor activities more comfortable.
Large, dome-shaped contact lenses can smooth the eye’s surface and sharpen vision for some people. A contact lens specialist can advise if they’re likely to help with your corneal haze. Not every approach works the same way for Fish-eye disease.
Handheld magnifiers, high-contrast settings, and screen readers can make reading, school, and work tasks easier. Vision rehabilitation teaches practical strategies at home and on the job.
When clouding is severe, a corneal transplant may restore clearer vision. Results vary, and grafts need lifelong eye care and regular checkups.
Your genes may have an impact on how drugs work for you
Some treatments for fish-eye disease, like lipid-lowering drugs, can work differently depending on your genes, which affect how your body absorbs, transports, or clears fats. Genetic differences may guide dose, choice of medication, or need for added therapies.
Pharmacological treatments
Fish-eye disease has no approved medicine that corrects the underlying enzyme problem, but a few drug options may help manage cholesterol levels or ease eye discomfort. Some ask whether medicines can change early symptoms of fish-eye disease like glare sensitivity or blurry vision; most drugs do not clear the corneal clouding. Treatment is individualized and guided by lipid levels, eye findings, and access to clinical trials. Your care team may combine supportive eye care with medicines that address LDL or triglycerides while monitoring safety.
Atorvastatin or rosuvastatin may be used if LDL cholesterol is high in fish-eye disease. They do not reliably raise HDL or clear corneal clouding, so expectations should be modest. Not everyone responds to the same medication in the same way.
Icosapent ethyl or omega-3-acid ethyl esters can lower high triglycerides, which some people with fish-eye disease may also have. These do not treat the enzyme deficiency or reverse corneal opacity.
Lubricating eye drops such as carboxymethylcellulose or sodium hyaluronate can ease dryness, burning, or light sensitivity. They help comfort but do not remove the lipid deposits causing the cloudy cornea.
Fenofibrate may be considered if triglycerides remain high despite diet changes. Effects on HDL are inconsistent in fish-eye disease, so lipid panels should be checked regularly.
Genetic influences
In Fish-eye disease, inherited changes in a gene called LCAT lower the activity of an enzyme that helps clear certain fats, including cholesterol, from the blood and the front of the eye. A “carrier” means you hold the gene change but may not show symptoms. Fish-eye disease follows an autosomal recessive pattern: most people develop it only when they inherit two changed copies of the gene, one from each parent.
When both parents are carriers, each pregnancy has a 1 in 4 (25%) chance of a child with Fish-eye disease, a 1 in 2 (50%) chance of a carrier, and a 1 in 4 (25%) chance of neither. Even within the same family, severity can differ because the exact gene changes and other factors can act like a dimmer switch on enzyme activity. Genetic testing for Fish-eye disease can confirm the cause and identify carriers, and genetic counseling can help you understand what the results mean for relatives.
Is Fish-eye disease genetic?
Genetics are central in Fish-eye disease. It’s caused by inherited changes in the LCAT gene, usually passed in an autosomal recessive pattern. Variations determine enzyme activity, severity, and family risk; carrier and diagnostic genetic testing can clarify inheritance and guide counseling.
Pharmacogenetics—how genetics influence drug effects
In Fish-eye disease, inherited changes in the LCAT gene reduce the enzyme that helps “mature” HDL, which shapes how medicines work and how doctors think about treatment of Fish-eye disease. Because the core problem is HDL formation, drugs that mainly try to raise HDL levels (for example, niacin or some fibrates) generally don’t fix the underlying issue, and a higher HDL number may not mean better HDL function. By contrast, medicines that lower LDL cholesterol, such as statins or ezetimibe, can still be useful to reduce cardiovascular risk drivers, with goals tailored to the individual. Alongside medical history and cholesterol results, genetic testing can sometimes identify how your body is likely to respond to certain lipid medicines. Differences in a common liver transport gene can also raise the chance of statin-related muscle side effects, so the choice or dose of statin may be adjusted if needed. Confirming the LCAT change that causes Fish-eye disease may also help determine eligibility for clinical trials of enzyme replacement or gene-based therapies, which are still under study.
Interactions with other conditions
When Fish-eye disease occurs alongside other conditions that affect the heart or eyes, the overall impact can be greater day to day. Doctors call it a “comorbidity” when two conditions occur together. The very low HDL cholesterol seen in Fish-eye disease can combine with high LDL cholesterol, high blood pressure, type 2 diabetes, or smoking to raise overall heart risk, even though the link between Fish-eye disease alone and early artery disease is mixed in studies. If someone also lives with another inherited lipid problem, such as familial hypercholesterolemia or elevated lipoprotein(a), the risks for plaque buildup may add up and call for more aggressive cholesterol lowering. Unlike the classic, complete form of LCAT deficiency, Fish-eye disease usually spares the kidneys, but existing kidney disease or diabetes-related kidney changes can complicate cholesterol management and may need closer monitoring. For someone whose early symptoms of Fish-eye disease were light sensitivity and blurry vision, coexisting dry eye or corneal surface problems can make glare and blur more noticeable, and eye procedures may need to account for a cloudy cornea. Many can still use standard heart medicines like statins to reduce LDL cholesterol; coordinating care between cardiology, ophthalmology, and genetics helps tailor treatment when conditions overlap.
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 hazy, glare-prone vision that worsened in bright light, especially around childhood. Families sometimes recalled a relative who avoided night driving or struggled with halos around streetlights. Before modern testing, these stories were often grouped with other corneal problems, since cloudy corneas can look similar from the outside.
From early theories to modern research, the story of fish-eye disease moved from careful observation to clear explanation. Early case reports noted a distinctive, milky ring in the outer cornea and significant light sensitivity, but eyesight could remain fairly good in the center for years. Doctors recognized that this pattern differed from more common corneal dystrophies, yet the cause remained unclear. As clinical photography and slit-lamp exams improved in the mid-20th century, descriptions became more precise, separating this condition from look-alikes that scar the cornea or raise eye pressure.
In recent decades, knowledge has built on a long tradition of observation. Blood tests began to show very low levels of a substance called HDL (“good” cholesterol) in people with fish-eye disease, linking an eye finding with a body-wide lipid change. This was a turning point: a corneal condition was now tied to how fats move and are processed in the bloodstream. Researchers then identified changes in a gene that makes an enzyme called LCAT, which helps HDL work properly. When LCAT activity is partly reduced, cholesterol can build up in the cornea, leading to the typical clouding seen in fish-eye disease. This genetic insight clarified why the cornea is affected while other organs are usually spared, distinguishing it from the more severe, full LCAT deficiency.
Once considered rare, now recognized as more widespread in certain families and regions due to better awareness and genetic testing, fish-eye disease has been reported across diverse populations. Naming has also evolved. Earlier labels emphasized the striking corneal appearance; later classifications placed fish-eye disease within a spectrum of LCAT-related conditions. This shift helped clinicians counsel families about inheritance, which follows an autosomal recessive pattern—meaning both parents quietly carry a nonworking gene copy.
Historical differences highlight why careful examination and modern tests matter. Past confusion with other corneal disorders sometimes led to unnecessary treatments that did not help. Today, the link between corneal findings, HDL levels, and LCAT variants guides accurate diagnosis. It also frames research into supportive care—such as light management and monitoring vision—and into whether future therapies that modify lipids or enzyme function might change the course. Knowing the condition’s history shows how everyday observations at the clinic slit lamp, paired with advances in genetics, shaped our current understanding of fish-eye disease.