In conclusion, we have verified our hypothesis that lamin A combined with the progerin-associated nuclear envelop strongly controls cell aging associated with DNA damage. The present study also reveals that some radiation-induced DNA damage could be related to a common mechanism underlying natural aging, and that the exaggerated aging phenotypes of HGPS are, in part, caused by a more rapid accumulation of such DNA damage, or by more frequent emergence of cells bearing such damages because of imperfect DNA repair. Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.