Indeed, studies have shown that a loss of AMPK accelerates aging-induced myopathy and mitochondrial dysfunction [35], and AMPK activation stimulates autophagy and ameliorates muscular dystrophy [36], FGF21 promotes myogenic differentiation and transformation of aerobic myofibers [37] via the AMPK pathway [38], and TNFα is known to inhibit AMP-activated protein kinase, leading to the reduction of oxidative capacity in skeletal muscle [39]. The gene discussed is FGF21; the disease is myopathy.