Also, atherosclerosis was not affected in Ldlr−/− mice with a BM p16INK4a-deficiency [62], despite the fact that p16INK4a is a regulator of macrophage activation and polarization and p16INK4a-deficiency reduces LPS-induced NF-κB activation in BM-derived macrophages [63]. This evidence concerns the gene LDLR and atherosclerosis.