Genetic or pharmacologic strategies blocking p65, the classical NF-κB DNA-binding subunit, or its upstream activator, IκB kinase β (IKKβ), have been found to reduce inflammation and accelerate muscle regeneration.1 This type of treatment approach is problematic for DMD patients, however, given the broad role of this transcription factor, particularly in immunity.3 This evidence concerns the gene NFKB1 and Duchenne muscular dystrophy.