Depletion of Treg in Apoe−/− or Ldlr−/− murine models aggravated atherosclerosis, with Treg suggested to limit plaque inflammation and disease progression, although the mechanisms responsible remain poorly defined.33–35 Data on Treg in human atherosclerosis are scant and fraught with contradictory findings. The gene discussed is LDLR; the disease is atherosclerosis.