Both transgenic overexpression of the anti-apoptotic protein Bcl2 and deletion of the pro-apoptotic protein Bax reduced muscular dystrophy in dyW/dyW mice (Girgenrath et al., 2004; Tables 4, 5) and removal of the mitochondrial calcium regulator cyclophilin D, which regulates mitochondrial permeability transition pore, attenuated muscular dystrophy in dyW/dyW mice (Millay et al., 2008; Table 5). This evidence concerns the gene BCL2 and muscular dystrophy.