Cardiotoxic drugs such as doxorubicin can induce premature senescence in cardiomyocytes as evidenced by increases in p16Ink4a and p53/p21Cip1/Waf1 expression, increased SA-ßgal signaling, decreased cardiac troponin I phosphorylation, and decreased telomerase activity [141,142], potentially contributing to doxorubicin-induced cardiomyopathy. This evidence concerns the gene CDKN1A and cardiomyopathy.