Similarly, although blocking farnesylation and thereby preventing the permanent farnesylation of progerin is sufficient to extend the lifespan of mouse models of HGPS (Varela et al., 2008; Zhang et al., 2013), blocking farnesylation with three different pharmacological and genetic approaches in C. elegans was sufficient only to improve the age-related nuclear morphology defects, but not the lifespan, of wildtype worms (Bar et al., 2009; Bar and Gruenbaum, 2010). Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.