NFKB1 and Hutchinson-Gilford progeria syndrome: Importantly, many of these pathways overlapped with those previously found to be misregulated based on studies in various cellular and mouse models of HGPS, including mTORC1 [26], Notch signaling [37], the UPR [29], Wnt/b-catenin signaling [28] and NF-kB[24], as well as pathways involved in myogenesis [45], oxidative phosphorylation [17] and apoptosis [46].