With the identification the canonical pathway that links the NLRP3 inflammasomewith IL-1/IL-6/CRP [180], targeting the NLRP3 inflammasome may providetherapeutic benefits in ASCVD, especially in light of the results of clinicaltrials such as CANTOS, which demonstrated that inhibiting inhibitingIL-1β, a main product of NLRP3 inflammasome activation, diminishedclinical endpoints in patients with atherosclerotic disease independent of lipidlevel lowering, accompanied by a reduction in IL-6 and CRP [66, 181]. Here, IL1B is linked to atherosclerosis.