NFKB1 and Hutchinson-Gilford progeria syndrome: Numerous studies have shown an increase in NF-κB activity with ageing; i.e., human fibroblasts from aged individuals and from patients with Hutchinson-Gilford progeria syndrome exhibit over-activation of NF-κB [48,49]; DNA binding to NF-κB is increased in the skin, liver, kidney, cerebellum, heart muscle, and gastric mucosa of elderly mice [50,51,52].