LMNA and Hutchinson-Gilford progeria syndrome: To what extent the deletion and/or the persistent farnesylation is the molecular basis to HGPS is unclear, as a mouse model of HGPS expressing the truncated, but non-farnesylated variant of Progerin still develop progeroid symptoms [15] and non farnesylated Progerin in human cells elicits the same DNA damage responses as farnesylated Progerin [16].