In another study, using transgenic mice expressing a constitutively active form of Ikkβ in muscle stem cells, a link between stem cell functional exhaustion and NF-κB-dependent telomere shortening was established in disease-related chronic injuries such as in Duchenne muscular dystrophy [173], suggesting that maintaining telomere length of muscle stem cells could improve its regenerative capacity also in normal and pathological ageing, not only in DMD. This evidence concerns the gene NFKB1 and Duchenne muscular dystrophy.