Preclinical studies highlighted in this review and summarized in Table 1 clearly show that the pathology of DMD can be alleviated by activating factors like PGC1α, PPARδ, ERRγ, AMPK, and SIRT1 that promote remodeling of skeletal muscle towards the slow/oxidative phenotype, which is more resistant to contraction-induced damage, or by inactivating factors like Fnip1, E2f1, cyclin D3, Nfix, and RAGE that repress this phenotype. The gene discussed is PPARGC1A; the disease is Duchenne muscular dystrophy.