In the present study we have focused our attention on the inflammatory cytokine interleukin-6 (IL-6), based on the evidences that (i) IL-6 increases in DMD patients compared with healthy subjects (10–12), (ii) high levels of IL-6 promote muscle proteolysis (13–15), (iii) selective modulation of inflammatory response ameliorates muscle pathology in mdx mice, reducing IL-6 (16) and (iv) inhibition of the IL-6 activity (17) and of the intracellular mediator, namely the JAK/STAT pathway, stimulates muscle regeneration in both aged and dystrophic mice (18,19). This evidence concerns the gene IL6 and Duchenne muscular dystrophy.