The inhibition of this axis acts as a non-canonical NLRP3 inflammasome pathway, which may protect endothelium function as well as prevent hypercholesterolemia induced atherogenesis (Koka et al., 2017); interestingly, NLRP3 inflammasome strikingly increase susceptibility of macrophages and migration upon lipid stimulation, which may finally promote atherosclerosis (Li et al., 2014). The gene discussed is NLRP3; the disease is familial hypercholesterolemia.