William syndrome is a syndrome characterized by cognitive deficits, mild mental retardation and arterial stenosis due to microdeletion of segment 7q11.23 on the long arm of chromosome 7 near the mitotic end, with an incidence of approximately 1/10,000. the pathogenesis is mainly the deletion of the critical region (WBSCR) of 7q11.23. the microdeletion of chromosome 7q11.23 can be of paternal or maternal origin. Almost all cases are sporadic. Clinical features: The main clinical features include mental retardation with microcephaly, peculiar facial features (thick lips, plump subcutaneous tissue around the eyes, low nasal bridge, strabismus, inner eye canthus, blue iris, long midperson, etc.), supra-aortic stenosis, short stature, renal vascular stenosis hypertension due to progressive connective tissue dysplasia, and joint dysfunction. Friendliness, talkativeness, and sociability, as well as hoarseness of voice, are characteristic behavioral abnormalities of the disease. Patients have mild to moderate intellectual impairment, with an IQ between 40 and 100, averaging 60; poor reading and writing skills and difficulty with even simple arithmetic; language skills that far exceed general cognitive abilities; auditory sensitivity and poor concentration, but amazing stamina for listening to music, singing, and playing musical instruments. Arterial stenosis is the characteristic abnormality of the disease, with supra-aortic stenosis being the most common, accounting for 75% of cases. Hypercalcemia can occur at any age, with idiopathic hypercalcemia in 15%, hypercalciuria in 30%, hypothyroidism in 10%, and a high incidence of diabetes mellitus in adulthood. Treatment: Before treatment, all examinations should be improved to clarify the lesions, and the corresponding symptomatic comprehensive treatment should be taken for the specific lesions. Various physical deformities can be corrected accordingly; for patients with severe cardiovascular and renal abnormalities, surgical treatment is feasible, which can help prolong life span and avoid secondary hypertension. Prevention: 1. For familial transmission of suspicious cases, prenatal amniotic fluid cell chromosome analysis and FISH testing are required. Fetal cases of supra-aortic stenosis detected by ultrasound detection are important for prenatal diagnosis. 2. Pay attention to dietary regulation. Patients with hypercalcemia need a low-calcium diet, steroids in severe cases, and close attention to the occurrence of renal calcium deposits.