To determine the impact of progerin expression in the endothelium on cardiovascular pathology in HGPS, we established mice expressing progerin exclusively in ECs by crossing transgenic mice carrying tet operon–driven wild-type or HGPS mutant (1824C>T; G608G) lamin A minigenes (32), with transgenic mice expressing a tetracycline-responsive transcriptional activator under the control of the endothelium-specific Cdh5 promoter (34). This evidence concerns the gene CDH5 and Hutchinson-Gilford progeria syndrome.