Repressing NF-κB activity is relevant in the context of dystrophinopathy: on one hand, NF-κB signaling is persistently elevated in DMD mouse models and patients [11], and suppresses the myogenic program [27, 28]; on the other hand, inhibiting this pathway has been reported to exert protective effects in mouse models of muscle injury [11, 42]. The gene discussed is NFKB1; the disease is neuromuscular disease caused by qualitative or quantitative defects of dystrophin.