Heart disease is the leading cause of death worldwide. One reason is that the heart is one of the least regenerative organs in the human body. When cardiac muscle is lost—for example, through myocardial infarction (heart attack)—the heart heals principally though formation of scar tissue (1). As a result, contractile function declines, and patients often progress to heart failure. Absence of regeneration in the heart has been attributed to the inability of muscle cells (myocytes) to undergo cell division, coupled with the absence of a muscle-producing stem cell population in the heart. Although the heart cannot effect whole-scale tissue regeneration, there is mounting evidence that some myocyte repopulation may occur. On page 98 in this issue, Bergmann et al.(2) provide strong evidence that cardiac myocytes can repopulate in the human heart, and they exploit one of the worst man-made environmental disasters to address this question.

During human fetal life, there is extensive proliferation of cardiomyocytes. From birth to adulthood, heart mass increases by about 30-to 50-fold (3). The nonmyocyte populations in the heart, such as vascular and connective tissue cells, contribute many new cells during postnatal growth. By contrast, cardiomyocyte proliferation slows dramatically around the time of