To examine the consequences of CGI-58−/− deficiency and the concomitant TG accumulation in myeloid cells on atherogenesis, we generated CGI-58flox/flox/ApoE−/− (designated ApoE−/−) and macCGI-58/ApoE-DKO mice and challenged them with a HF/HCD to induce lesion formation. The gene discussed is APOE; the disease is hydrops fetalis.