By adequately addressing the pathway alteration described here, new approaches to regulate muscle damage in Duchenne muscular dystrophy can be envisaged; for instance, treatment with drugs that will interfere with Cav1.1, Panx1 or P2Y receptors will decrease the effect of increased ATP release and are candidates to normalize the expression of pro-apoptotic genes [75]. The gene discussed is PANX1; the disease is Duchenne muscular dystrophy.