Particularly, (1) we compared the efficacy of RvD2 to a standard drug (prednisone) for which the effects are already known; (2) we assessed recognized key parameters (grip strength, hang test, ex vivo isometric force, and validated immunohistological measurements) using standard operating procedures; and (3) we used two different mouse models of DMD, the well-characterized dystrophin-null mice (mdx mice) that recapitulate the genetic mutation observed in humans, and the utrophin-dystrophin double knockout mice (mdx-utrn dKO mice) that mimic more closely the severity of the human disease. This evidence concerns the gene DMD and Duchenne muscular dystrophy.