Increased protein degradation and impaired muscle function are linked to elevated oxidative stress in muscles [82] and this can lead to muscle atrophy by inducing p38 MAPK/myogenin axis activation and STAT3-dependent degradation of MyoD1 (myoblast determination protein 1) in various disorders such as muscular dystrophies, aging and sarcopenia as well as disuse atrophy [83]. The gene discussed is MYOD1; the disease is muscular dystrophy.