In summary, our data based on the genetic deletion of CD38 and its pharmacological inhibition in different DMD models (i) clearly indicate that CD38 is an important contributor to the NAD+ deficit and to the Ca2+ dysregulation, two major features in this disease, and (ii) strongly support our innovative strategy to treat DMD by a single common pharmacological approach reducing simultaneously the Ca2+ overload and the NAD+ deficit, leading to an important improvement in the DMD phenotype. This evidence concerns the gene CD38 and Duchenne muscular dystrophy.