A study using mouse models of mild and severe DMD (dystrophin-deficient and dystrophin/dystrophin double KO, respectively) found significantly reduced levels of Panx3 in the dystrophic muscles of these mice, suggesting dysregulation of Panx3 expression in DMD.139 Based on these findings, targeting Panx1 channel activity to reduce ATP release may hold potential for benefiting DMD patients, although further research is needed to confirm this. This evidence concerns the gene PANX3 and Duchenne muscular dystrophy.