This intriguing finding is consistent with the studies in mouse models that have shown that loss of nuclear hormone receptor 77 (NUR77) or Krüppel-like factor 4 (KLF4), two factors associated with lower macrophage inflammation (i.e., a more “M2-like” phenotype) leads to more plaque inflammation and atherosclerosis progression (159–163). The gene discussed is KLF4; the disease is atherosclerosis.