To investigate how LDAH gain-of-function affects atherosclerosis development, we generated myeloid-specific LDAH transgenic (LDAH-Tg) mice under the control of the promoter and enhancer of the mouse Csf1r locus, which direct position and copy number-independent expression in macrophages and granulocytes (Fig. 1A)15,16. The gene discussed is LDAH; the disease is atherosclerosis.