Activation of NLRP3, in turn, results in the secretion of the pro-inflammatory cytokine IL-1β.This pathway appears to be necessary for atherosclerosis progression, as LDL receptor (Ldlr)-/- mice, transplanted with bone marrow cells deficient in IL-1β or in components of the NLRP3 inflammasome, had reduced plaque progression (31, 34). This evidence concerns the gene LDLR and atherosclerosis.