The discovery by Duewell et al. [52] in 2010 that low-density lipoprotein receptor (LDLR)−/− atheroprone mice exhibit diminished atherosclerotic lesions consequent to their lack of NLRP3, ASC or IL-1α/β in bone marrow cells yielded the first concrete evidence that the NLRP3 inflammasome contributes to the onset of atherosclerosis [48,52]. This evidence concerns the gene LDLR and atherosclerosis.