Moreover, in our mouse model of Dox-induced cardiomyopathy, we found that AAV9-mediated Redd1 overexpression aggravated Dox-induced cardiac function, SASP-related cytokine production, and the expression of senescence markers (i.e., p16INK4a and p21) in cardiomyocytes. Here, CDKN2A is linked to cardiomyopathy.