LDLR and atherosclerosis: Additionally, CXCL16 significantly contributes to the progression of atherosclerosis (47), as evidenced by the observation that mice deficient in both CXCL16 and LDLR (CXCL16−/− low density and low intensity −/−) exhibit exacerbated atherosclerotic lesions primarily due to impaired cholesterol efflux caused by dysfunctional CXCL16 receptor activity (47, 48).