CVB3-mediated cleavage of dystrophin, which drives altered sarcolemmal structure, may contribute to altered Cx43 dynamics: in cardiac tissue from Duchenne muscular dystrophy (DMD) patients and mouse models, both lacking functional dystrophin, increased Cx43 expression and lateralization away from the ID have been observed [82]. This evidence concerns the gene GJA1 and Duchenne muscular dystrophy.