Actually, besides excessive S-nitrosylation, other NO-mediated mechanisms concur to muscular atrophy, which we cannot exclude might also play a role in GSNOR-deficient systems, such as: (1) deactivation of cGMP signaling, which is extremely important to sustain vasodilation1,26 and stimulate satellite cells proliferation9; (2) deregulation of Ca2+ uptake/release for sarcoplasmic reticulum1,33; (3) impairment of mitochondrial biogenesis and metabolism34. This evidence concerns the gene ADH5 and muscular atrophy.