Hepatolenticular degeneration (HLD), or Wilson’s disease (WD), is a chronic progressive disorder of copper metabolism inherited in an autosomal recessive manner. The gene is located at 13q14.3 and encodes a P-type ATPase, which is involved in the metabolic process of copper transport across the membrane. It is believed that WD is caused by mutation of the gene that reduces or loses the function of this enzyme, resulting in abnormal copper metabolism, slowed hepatic synthesis of copper blue protein, significantly reduced biliary copper excretion, copper deposition in the liver, brain, kidney, joints, blood cells and cornea, causing clinical symptoms of damage to the corresponding organs. The main clinical manifestations are hepatocellular damage, degenerative brain lesions and corneal K-F rings of varying degrees. WD is one of the most common neurogenetic diseases with a prevalence of 0.5-3/100,000 in the world population. Its prevalence has regional differences, with a low prevalence in the European and American populations, a high prevalence in countries and regions such as Eastern Europe and Israel, and a high prevalence in Japan, Korea and Southeast Asian countries, and a significantly higher prevalence in China than in the above-mentioned countries or regions. Because of the large population base in China, the absolute number of diseases is large and the harm caused is also large, so it is of great theoretical and practical significance to strengthen WD research. WD is one of the treatable genetic diseases, and early diagnosis and standardized treatment can often prevent serious irreversible damage to important tissues and organs, and allow patients to live, learn, work and live as long as healthy people.