Furthermore, a causal link between progerin and CRM1 overexpression was demonstrated because ectopic expression of progerin in HeLa cells elicited elevated CRM1 levels, at least in part through enhancing the binding activity of NF‐YA (a positive transcription factor) to the CRM1 promoter region, and because treatment of HGPS cells with FTI that decreased progerin levels resulted in turn in downregulation of CRM1. Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.