Although the underlying mechanism is unclear, activation of PPAR-β/-δ in skeletal muscle, which has a significant role in insulin sensitivity, has been proposed to account for the beneficial metabolic effects of PPAR-β/-δ agonists on lipid profile and insulin resistance, possibly as a result of increased fatty acid catabolism, cholesterol efflux, energy expenditure [153–157], and oxidative capability [155] in the muscle. The gene discussed is INS; the disease is Insulin resistance.