When a diagnosis of cardiotoxicity is strongly suspected, confirming the etiology as anthracycline-induced in nature may be challenging, short of exclusion, given the rarity of the disease and its clinical presentation. Regarding the agents used in this case, doxorubicin is known to cause cardiotoxicity related to myocardial damage in as many as10—26% of cancer patients. Studies have shown that after completion of anthracycline therapy, 65% of survivors of childhood leukemia develop progressive cardiotoxicity after 6 years. The pathophysiology of cardiotoxicity in longterm survivors is characterized by reduced left ventricular wall thickness and mass, which is indicative of decreased cardiac muscle and depressed left ventricular contractility, itself indicative of unhealthy heart muscle. The occurrence of anthracycline-induced cardiotoxicity is progressive from the first dose, but in some individuals rapid deterioration in cardiac function can be found even at low doses. The adverse effect, which is directly related to the cumulative (total) dose of anthracyclines received, is irreversible. Once CHF has occurred after anthracycline administration, the mortality rate can exceed 50% within 2 years of treatment cessation. In our patient, chemotherapy-induced CHF was characterized by a cumulative anthracycline dose of 563 mg/m2over the previous 4 years in the absence of any known cause of cardiomyopathy and with evidence of multi-organ involvement directly attributable to the ALL or otherwise unexplained in the clinical setting.