Interestingly, activation of the NLRP3 inflammasome is considered central to the onset and progression of “inflammaging”, a condition characterized by self-perpetuating low-grade inflammation that drives a series of alterations (including atherosclerosis, myocardial fibrosis, sarcopenia, and neuronal dysfunction with consequent apoptosis) which are a hallmark of the transition from normal aging to frailty and disability. This evidence concerns the gene NLRP3 and atherosclerosis.