While these endpoints in most of the above clinical trials typically assess dystrophin expression and improvements in muscle function through measures such as the North Star Ambulatory Assessment (NSAA) score, Time to Rise, 10-m Walk/Run, stride velocity at the 95th percentile, and 100-m Walk/Run, etc., we hypothesize that in the inflammatory and immune-reactive environment inherent to DMD, treatments may not achieve optimal efficacy unless this inflammation is effectively managed. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.