A mild, persistent and familial unconjugated hyperbilirubinemia was described by the French physician Gilbert in 1907, and subsequently many cases of icterus intermittent juvenilis, familial non-hemolytic bilirubinemia, and constitutional non-hemolytic bilirubinemia have been reported. hemolytic jaundice, hereditary non-hemolytic bilirubinemia, and constitutional hepatic dysfunction. constitutional hepatic dysfunction, constitutional hyperbilirubinemia, and juvenile intermittent icterus. In this syndrome, there are no abnormalities in liver function other than the possible jaundice and rise in unconjugated bilirubin, and all tests are normal, with little or no significant symptoms. This difference in sexuality may be related to sex hormones, even though in the general young population, women have lower bilirubin values than men, making the female prevalence rate likely to be underestimated. The percentage of the population varies according to regional studies, and it is possible that 2-5% of the population in Europe and the United States has this syndrome. The clinical features of this syndrome are often detected around the time of puberty or in early adulthood, and most people are found to have higher than normal total bilirubin and unconjugated bilirubin concentrations during a physical examination or routine biochemical tests. The serum total bilirubin values fluctuate, ranging from 1.2 to 3 mg/d of g, and rarely exceed 5 mg/dl, and there are not only daily variations, but also seasonal differences have been reported, and a small number of women with Gilbert’s variant have increased yellow bile before menstruation. The mechanism of abnormal bilirubin metabolism in Gilbert’s disease is quite complex, and in about 40% of patients, the t-blood cell survival rg is shorter than in the general population, but] there is a specific cause of hemolysis, and such hemolysis is not sufficient to explain this rise in indirect bilirubin. It has been suggested that this syndrome is mainly due to insufficient levels of bilirubin glucuronosyltransferase in the fine thorax of the liver, or a lesser capacity to act, allowing a poorer rate of clearance of serum schema-conjugated rationale bilirubin. Recent advances in genetic molecular science have given me some more insight into this disease. Early on, it was thought to be auto-dominant, but in recent years, it is thought to be recessive and hereditary. It is mainly due to genetic abnormalities, probably heterozygous with a single mutated gene. It is mainly related to the mutation of the bilirubin-hemoglobin glucuronosyltransferase gene (UGT-1A1) in its initiation region, which may be as high as 30% in Africans and only about 3% in Asians. Some studies have also pointed out that another variation in the UGT-1A1 gene may be the cause of Gilbert’s disease in Asian populations. Perhaps the genetic changes that alter this enzyme are not identical in people with Gilbert’s disease, which may indicate that the results of studies on this disorder are not identical, but the different genetic changes affect the same enzyme, causing the same increase in serum unlike bilirubin. In addition, surgery, fever, infection, overexertion, alcohol consumption, and other stressful situations may also increase. Conversely, increasing the intake of calories, t can improve the disease. On pathological examination, liver function is normal and hepatocyte bilirubin is not abnormal in those with this syndrome. Biochemical examinations show few abnormalities, except for a mild increase in unconjugated bilirubin in the blood. Although this syndrome is not a significant problem, some scholars believe that it is somehow associated with neonatal jaundice and that some drugs with a similar metabolic pathway to bilirubin may also be affected.