It has recently been shown that genetic or pharmacological inactivation of TRPC6 with the small molecule BI 749327 results in improving skeletal and cardiac morphology and dysfunction, and reducing skeletal and bone deformities in mice lacking both dystrophin and utrophin (mdx/utrn–/– double knockout (dko) mice) representing a severe DMD model [50]. Here, UTRN is linked to Duchenne muscular dystrophy.