Nie et al found that [71], mice with GPR116 selectively knocked out in AT were more susceptible to impaired glucose tolerance and insulin resistance induced by high-fat diet, and showed increased levels of circulating triacylglycerol, increased ectopic lipids in liver and skeletal muscle, and increased levels of inflammatory factors, suggesting that the FNDC4-GPR116 axis is closely related to systemic insulin resistance. The gene discussed is FNDC4; the disease is Insulin resistance.