In conclusion, ApN retains its beneficial properties in dystrophic muscles by activating AdipoR1 and the AMPK-SIRT1-PGC-1α pathway, thereby inducing a shift in the secretion of downstream myokines toward a less inflammatory profile while upregulating utrophin A. ApN as well as its downstream myokines may be therapeutic targets for the management of DMD. The gene discussed is ANPEP; the disease is Duchenne muscular dystrophy.