Proposed mechanisms include inhibition of platelet-derived growth factor receptor, VEGF, or KIT receptors, as well as caspase-activated mitochondrial apoptosis that leads to direct injury of myocytes.8 In addition, this cardiotoxicity may be exacerbated by hypertension and hypothyroidism.8 In our case, there was no evidence of hypertension throughout the treatment period. The gene discussed is VEGFA; the disease is hypertensive disorder.