Previous studies demonstrated that LTBR recruits leucocytes, which may have a causal role in islet destruction42; increased EDN1 correlates to glucose intolerance and insulin resistance in mice with high-fat diet as well as intermittent hypoxia43,44; NOS2, a known mediator of beta cell dysfunction, is also a target of NF-κB proinflammatory signaling pathway45; HK1 impairs glucose metabolism to induce high basal insulin secretion from the beta cells46; TEK, an angiopoietin receptor, and its ligands are involved in the diabetes progression47. Here, INS is linked to Glucose intolerance.