Under oxidative stress, NADPH oxidase is a major source of ROS, and its enhanced activity increases the activity of src kinase, the expression of TRPC1 and, subsequently, the mechanosensitive entry of Ca2+ through TRPC1 (rather than SOCE through TRPC1), which is believed to be a key mechanism for muscle damage and functional impairment during the pathogenesis of DMD [38,185]. The gene discussed is TRPC1; the disease is Duchenne muscular dystrophy.