Other mechanisms involve an altered prostaglandin E2 (PGE2) pathway that may promote or restrict beta-cell proliferation and survival via EP2 receptors, and gut microbiota dysbiosis affecting insulin sensitivity through microbial metabolites such as short-chain fatty acids (SCFAs), which enhance glucose homeostasis, or branched-chain amino acids, which activate mammalian/mechanistic target of rapamycin (mTOR) and contribute to insulin resistance [4]. The gene discussed is INS; the disease is Insulin resistance.