In HGPS, it has been proposed that altered nuclear shape (herniation) is attributed to the accumulation of farnesylated progerin on the nuclear lamina as it can be rescued via treatment with farnesyl transferase inhibitors (FTIs); the rescue of the misshapen nucleus by reducing prelamin A or progerin from the nuclear lamina ameliorates senescence in HGPS cells [6,7] and progeroid features in progeria mouse models [7-9]. This evidence concerns the gene LMNA and Hutchinson-Gilford progeria syndrome.