TopIIα, highly expressed in cancer cells and required for cell division, is the target for anthracycline’s antitumor effect.40–42 However, adult cardiomyocytes express only TopIIβ, which is not required for cell division.43 Since dexrazoxane binds to TopIIβ and inhibits Dox-induced DNA double-strand break, it is likely that Dox causes cardiotoxic effects by targeting TopIIβ in cardiomyocytes.39 By binding to TopIIβ in the nucleus and stabilizing this enzyme, Dox causes continuous DNA breakdown and prevents the broken DNA double helix from repairing. The gene discussed is TOP2B; the disease is cancer.