1, congenital non-hemolytic jaundice is a group of hyperbilirubinemia caused by genetic defects due to impaired uptake, transport, binding or excretion of bilirubin by hepatocytes. 2, according to the nature of bilirubin in the blood, can be divided into two categories: (1) non-conjugated bilirubin increased type, there are Gilbert syndrome, Crigler-Najjar syndrome, Lucey-Driscoll syndrome; (2) conjugated bilirubin increased type, there are Dubin-johnson syndrome, Rotor syndrome. (3) Gilbert syndrome: hereditary unconjugated bilirubin elevation, an autosomal recessive disorder, prevalent in adolescents, patients with insufficient glucuronosyltransferase activity affecting the binding of unconjugated bilirubin in hepatocytes, resulting in a double defect in the uptake and binding function of unconjugated bilirubin by hepatocytes, generally does not require special treatment. 5, Dubin-Johnson syndrome: also known as chronic idiopathic jaundice, for hereditary increased conjugated bilirubin type I, is an autosomal recessive disorder, common in young people, with a family history; due to the capillary bile ducts of organic anion transport disorders, resulting in the operation of conjugated bilirubin from the hepatocytes to the capillary bile ducts is impaired, the result of conjugated bilirubin backflow into the blood, conjugated bilirubin level The level of conjugated bilirubin increases and the patient develops chronic or intermittent jaundice. 6.Rotor syndrome: It is a hereditary hyperbilirubin type II, due to a congenital defect in the uptake of free bilirubin and excretion of conjugated bilirubin by hepatocytes, resulting in a predominantly high level of conjugated bilirubin in the blood. It is autosomal recessive, and patients are mostly under 20 years of age, with no difference between men and women, and the prognosis is good. 7, Crigler-Najjar syndrome: also known as congenital glucuronosyltransferase deficiency. It is a rare, hereditary hyperbilirubinemia that occurs in newborns and infants and is divided into type I and type II. Type I is rare, and newborns often show bilirubin encephalopathy (nuclear jaundice) with muscle spasms and ankylosis, convulsions, and keratoconus within 2 weeks of birth, and most die in the first 18 months of life; Type II is rare, and is a partial deficiency of glucuronosyltransferase that does not disappear. The disease is lighter than type I, no neurological symptoms, normal intellectual development, and bilirubin encephalopathy is rare. Key points: 1, this group of diseases is genetic defects caused by elevated serum bilirubin levels. 2, there are mainly 5 diseases. 3, according to the clinical symptoms, the level and type of bilirubin elevation, the age of onset to identify the group of diseases. 4, Most congenital jaundice has a good prognosis and does not require treatment. 5.Histopathology of liver biopsy can be helpful in diagnosing this group of diseases.