High cortisol increases glycogenolysis, gluconeogenesis, and insulin resistance in the liver and muscle both indirectly (via increased lipolysis and proteolysis, thus increased fatty acids and amino acids, respectively) and directly (via counteraction on the insulin receptor) and increases visceral obesity and decreases insulin secretion; all of these effects, per se, can jointly lead to T2D and metabolic traits [73]. The gene discussed is INSR; the disease is Insulin resistance.