Heart failure due to myocardial infarction is the leading cause of morbidity and mortality in developed countries. 1 While that point needs no reiteration for the Circulation audience, its corollary does: that heart failure, in essence, is a myocyte-deficiency disease. Cell death, whether from acute infarction alone or from sustained sporadic losses in chronic heart failure, is not matched by sufficient cell replacement. Adult cardiac muscle cells have long lost much if not all of their capacity for proliferative growth, and differences in interpretation hinge on shadings between “none” and “almost none.” 2, 3 What cell replacement does occur occurs by other means, including the recruitment of undifferentiated progenitor cells—eg, from their niche in bone marrow through the circulation to the injured myocardium. 4