This cleavage results in the formation of mature unfarnesylated lamin A. Mechanistically, the mutation in lamin A gene found in HGPS (G608G) activates a cryptic RNA splice donor site, causing an internal deletion of 50 amino acids from prelamin A. This truncated, farnesylated prelamin A variant (progerin) fails to undergo cleavage resulting in accumulation in HGPS patients (Worman and Michaelis, 2018). Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.