We demonstrated that the overexpression of IL-6 in dystrophic mdx mice (mdx/IL-6 murine model) induced the exacerbation of the dystrophic phenotype at 24 weeks of age, the stage in which the classical mdx model shows a stabilization of the disease [45], whereas the inhibition of IL-6 signalling in dystrophin-deficient mice reduces ROS accumulation, myonecrosis, and inflammation in the diaphragm muscle, which represents the most compromised muscular district in DMD [28, 36, 37, 46]. This evidence concerns the gene IL6 and gas gangrene.