TRPC6 and cardiomyopathy: Different missense mutations in TRPC6 have been shown to result in excess calcium influx, largely by gain-of-function mutations (22), leading to the hypothesis that individuals carrying TRPC6 variants could be at increased risk of doxorubicin-induced cardiotoxicity and cardiomyopathy and perhaps be candidates for TRPC inhibition as a cardioprotective strategy.