Moreover, in cardiac muscle and myocytes from DMD mice lacking dystrophin and haplodeficient for utrophin (mdx/utrn+/– [HET] mice), TRPC6 mediates an abnormal rise in Ca2+i induced by acute mechanical stress, resulting in excessive force generation and arrhythmia (4). The gene discussed is UTRN; the disease is Duchenne muscular dystrophy.