For these reasons, we note that future studies in mice bearing distinct immune cell-specific deletion of Diaph1 in the absence of Ldlr, such as in myeloid cells or T lymphocytes, should directly uncover if myeloid Diaph1 contributes to atherosclerosis and if such findings are dependent- or independent of differences in plasma/liver content of cholesterol and triglyceride. The gene discussed is DIAPH1; the disease is atherosclerosis.