In DMD (muscular dystrophy on X chromosome, mdx) mice, we have shown that dystrophin deficiency caused post-translational remodeling of the cardiac ryanodine receptor (RyR2) macromolecular complex, due to S-nitrosylation and Calstabin2 (FKBP12.6) depletion, which leads to intracellular diastolic Ca2+ leak and ventricular arrhythmias (Fauconnier et al., 2010). This evidence concerns the gene RYR2 and Duchenne muscular dystrophy.