We demonstrated that pharmacological blocking of CRM1 using LMB mitigated an array of senescent marks in HGPS fibroblasts, and consistent with a key role for the CRM1‐mediated nuclear export in HGPS, overexpression of CRM1 lead rapidly normal fibroblasts to senescence (García‐Aguirre et al. 2019). This evidence concerns the gene XPO1 and Hutchinson-Gilford progeria syndrome.