The ischemic phenotype inspired multiple studies aimed at targeting the nNOS-NO pathway in DMD patients based either on the expression of dystrophin minigenes to provide the nNOSμ binding site, direct overexpression of the nNOS gene, supplementation with L-arginine (nNOS substrate), delivery of NO-donating drugs, or inhibition of phosphodiesterase 5A (PDE5A) to prolong the half-life of cGMP [72]. The gene discussed is PDE5A; the disease is Duchenne muscular dystrophy.