Cell-specific deletion of the mPGES-1 revealed that PGE2 formation in macrophages appears to be essential in this process: Mice lacking mPGES-1 expression in myeloid cells showed markedly reduced atherogenesis in an LDL-R (-/-), high fat-fed model, whereas depletion of mPGES-1 in vascular-smooth muscle or endothelial cells did not alter development of atherosclerosis in this mouse model [35]. This evidence concerns the gene PTGES and atherosclerosis.