On the cover: Complementary dystrophin and utrophin expression prevents dilated cardiomyopathy in aged mdx mice. The loss of cardiac dystrophin leads to dilated cardiomyopathy in human patients and very old mdx mice. It is currently not clear whether partial dystrophin expression can restore heart function. This image is a double immunofluorescence staining of the carrier mouse heart. Carrier mice express dystrophin in only 50% of their cardiomyocytes. Interestingly, utrophin (a functional homolog of dystrophin) is up-regulated in dystrophin negative cells of the carrier mouse heart. This complementary dystrophin and utrophin expression normalizes the anatomic defect and physiological dysfunction in the heart. This finding raises the hope of ameliorating dystrophin-deficient cardiomyopathy through partial gene and/or cell therapy. Dystrophin positive cells were revealed with a polyclonal antibody (green color). Utrophin positive cells were revealed with a monoclonal antibody (red color). Nuclei were visualized through DAPI staining (blue color). See related article, page 121.