In accord with these erudite observations, Velpongsa and Yeh [2] propose that inhibiting and deleting Top2β in the heart should be tested as a strategy for the primary prevention of anthracycline-induced cardiotoxicity, and in a recent review, Moudgil and Yeh [3] conclude that Top2β is required to initiate the entire phenotypic cascade of doxorubicin-induced cardiomyopathy. This evidence concerns the gene TOP2B and cardiomyopathy.