Taken together, our data suggests mTORC1, the UV response, apoptosis, the UPR and TNFα signaling via NF-κB pathways as immediate targets of progerin, whereas oxidative phosphorylation, Notch signaling and Wnt/b-catenin signaling likely reflect adaptive or compensatory pathways to long-term progerin expression in vivo in HGPS patients. Here, NFKB1 is linked to Hutchinson-Gilford progeria syndrome.