Interestingly, a recent study showed that apoE expression in the monocytes and macrophages of hypomorphic apoE mice deficient in LDLR expression (Apoeh/hLDLR−/− mice) attenuated nuclear factor kappa B (NF-κΒ)-dependent inflammation and atherosclerosis by enhancing cellular miR-146a levels [91]. The gene discussed is LDLR; the disease is atherosclerosis.