This uncoupling of ER stress and insulin resistance in HFD-fed Klf15−/− mice is explained by the possible induction of 5′-AMP-activated protein kinase (AMPK) and inhibition of mTORC1 signaling and stimulation of PGC-1α, leading to increased fatty acid oxidation [85]. The gene discussed is PPARGC1A; the disease is Insulin resistance.