In addition, heterozygosity of p65/RelA in a mouse model of Hutchinson-Gilford Progeria Syndrome (Zmpste24-/-) resulted in attenuated aging pathology and a prolonged lifespan, linked in part to a reduced systemic inflammatory response and a reduction in ATM/NEMO-mediated NF-κB activation [34]. This evidence concerns the gene NFKB1 and Hutchinson-Gilford progeria syndrome.