On molecular level, DOX affected several previously well-described mechanisms of DOX-induced cardiotoxicity including decreases in the expression of genes involved in intracellular calcium metabolism, Serca2a and RyR2 [13, 14, 16] and increases in Anp and Mmp2 levels, consistent with observations in the human heart failure [47–50]. The gene discussed is RYR2; the disease is heart failure.