The inflammatory response to fibre damage in DMD is an engaging candidate mechanism for disease worsening and different steps of inflammatory cascade, such as B-4, COX, LOX, MAPK, TNF-α, reactive oxygen species, and nuclear factor-κB signaling factors, are considered possible therapeutic targets to be joined with exon skipping therapy or protein restoration therapy [11, 26–28]. The gene discussed is TNF; the disease is Duchenne muscular dystrophy.