Through a variety of mechanisms, including increased energy extraction from food, distorted fatty acid metabolism, particularly short-chain fatty acids (SCFAs), altered adipose tissue composition and sensitivity to insulin, metabolic endotoxemia, increased systemic inflammation, and intestinal permeability, human research and animal models have linked this change in gut microbiota to the pathogenesis of obesity, insulin resistance, and subsequently T2DM [10-13]. The gene discussed is INS; the disease is Insulin resistance.