The pathophysiological significance of Cx43 S-nitrosylation is illustrated in a mouse experimental model of Duchenne muscular dystrophy in which the opening of Cx43 hemichannels by NO-mediated S-nitrosylation led to cardiac stress-induced arrhythmias (Lillo et al., 2019). This evidence concerns the gene GJA1 and Duchenne muscular dystrophy.