Although it has been reported that the onset of Dox-induced cardiomyopathy is caused by oxidative stress produced by Dox itself [44], Shimauchi et al. recently reported that Dox induces the expression of the Ca2+ transient receptor potential canonical (TRPC3), which is present in the myocardial cell membrane, and enhances ROS production from Nox2, resulting in the atrophy of cardiomyocytes [9]. Here, TRPC3 is linked to cardiomyopathy.