Interestingly, DMD-CCs exhibited a similar relative expression of known cardiac markers, and with trending increased Connexin 43 expression, similarly observed in mdx and mdx:utr CMs as a remodeling mechanism following functional dystrophin absence, with potential fatal arrhythmias in presence of β adrenergic stimulation (Patrick Gonzalez et al., 2015). This evidence concerns the gene DMD and Duchenne muscular dystrophy.