(2020) demonstrated that NLRP3 contributes to atherogenesis in a sex-dependent manner via estrogen-mediated regulation: their study demonstrated that ovariectomy condition in a valuable model of atherosclerosis, such as the low-density lipoprotein receptor gene knockout mice (Ldlr-/-), revealed that NLRP3 deficiency markedly reduced plaque formation in middle-aged females, lowering caspase-1 activation, IL-1β release, and immune cell infiltration. Here, LDLR is linked to atherosclerosis.