On the cover: c-kit is required for cardiomyocyte terminal differentiation. In adult mammalian hearts, the loss of cardiomyocyte proliferative potential—that is, cardiomyocyte terminal differentiation—restricts the heart to adaptation by growth through cardiomyocyte and left ventricular hypertrophy, a response associated with increased mortality. These images are immunofluorescent stains of isolated cardiomyocytes from 4-day-old and adult wild-type mice hearts. Neonatal cardiomyocytes (left panel) express c-kit (red), the transmembrane tyrosine kinase receptor for stem cell factor, but adult cardiomyocytes do not (right panel). Cardiomyocytes were visualized through α-myosin heavy-chain staining (green color), and nuclei were visualized through DAPI staining (blue color). Cardiomyocyte c-kit expression in neonatal cardiomyocytes is coincident with the onset of cardiomyocyte terminal differentiation, which is not seen in mice with genetic c-kit dysfunction. This finding raises the hope of regulating cardiac regeneration in adult hearts by interfering with c-kit signaling. See related article, page 677.