The mechanisms by which the elevated levels of FFAs decrease insulin sensitivity include inhibition of insulin-stimulated glucose transport [65], lipotoxicity hypothesis [66] that results in impairment of insulin secretory function through toxic effects on pancreatic β-cells, and finally increased lipolysis of the visceral adipose tissue and subsequent flux of FFAs to the nonadipose tissue leading to excessive endogenous glucose production and progression of insulin resistance and T2DM [67]. The gene discussed is INS; the disease is Insulin resistance.