XPO1 and Hutchinson-Gilford progeria syndrome: We show for the first time that the CRM1‐driven nuclear protein export mechanism is abnormally enhanced in HGPS fibroblasts and that this novel hallmark is critically involved in the disease, because pharmacological inhibition of CRM1 rescues the HGPS cellular phenotype and exogenous overexpression of CRM1 recapitulates HGPS in normal fibroblasts.