The prevailing assumption that loss of cardiac myocytes via apoptosis would contribute to the loss of cardiac pump function and, therefore, is undesirable, is highly plausible, but untested in mechanistic terms. Four potential counterexamples are discussed: altruistic cell sacrifice, genome surveillance, cell cycle surveillance, and immunological surveillance. Despite the logic underlying the proposed use of antiapoptotic drugs or genes as countermeasures in heart failure, these considerations suggest the need for vigilance to avoid unforeseen complications...