LMNA and Hutchinson-Gilford progeria syndrome: Fibroblasts taken from individuals with HGPS exhibit defective lamin A processing and accumulate a permanently farnesylated, truncated form of prelamin A termed progerin that induces abnormal nuclear morphologies and elevated levels of DNA damage (Liu et al., 2005) that are thought to contribute to disease pathologies (McClintock et al., 2006).