Based on these findings, we conclude that exacerbated atherosclerosis and its complications in Apoe−/−LmnaG609G/G609G and Ldlr−/−LmnaG609G/G609G mice are bona fide effects of progerin expression, independent of the genetic manipulation required to establish an atherosusceptible environment in preclinical mouse models. Here, LDLR is linked to atherosclerosis.