A team led by scientists from the Medical Research Council of the University of Cambridge in the UK conducted whole exome sequencing of body mass index (BMI) in over 500000 individuals. The results showed that mutations in the BSN and APBA1 genes had the greatest impact on obesity risk. The variation of BSN gene will increase the risk of obesity by six times, and is also related to the increased risk of nonalcoholic fatty liver disease and type II diabetes. The relevant research paper was published in the latest issue of the journal Nature Genetics. The research team used data from the UK Biobank and others to identify the two genes known to have the greatest impact on obesity, BSN and APBA1. Research has shown that one out of every 6500 adults has a BSN gene mutation, which may affect approximately 10000 people in the UK. Previous studies have identified several genetic variations associated with obesity, which have been active since childhood through the leptin melanocortin pathway in the brain, which is crucial for appetite regulation. However, unlike previously identified obesity genes, variations in BSN and APBA1 are only associated with adult obesity and not with childhood obesity. Moreover, the latest research suggests that BSN and APBA1 play a role in signal transduction between brain cells. Researchers believe they may have discovered a new biological mechanism of obesity: age-related neurodegenerative disorders may affect appetite control. However, they currently do not know whether BSN and APBA1 are involved in the leptin melanocortin pathway. The gene variation found in BSN has had the largest impact on obesity, type II diabetes and fatty liver observed so far, and highlighted a new biological mechanism to regulate and control appetite, giving researchers a new understanding of the relationship between genetics, neurodevelopment and obesity. (Lai Xin She)