What can be said, thus far, is that protection from DOX occurred in both quiescent and proliferative cardiomyocytes (hPSC-CMs, versus H9c2 myoblasts), and therefore is unlikely due merely to the absence or presence of cell cycling, and that susceptibility to DOX remained in cancer lines, both in the absence and presence of wild-type p53, a gene known to mediate the cardiac toxicity64. This evidence concerns the gene TP53 and cancer.