Although this remains to be tested genetically, in an apolipoprotein E-deficient mouse model of atherosclerosis, it has been shown that myeloid-specific deletion of ADAM17 resulted in significant increases in atherosclerosis development with a decrease in lesional macrophage area while endothelial-specific ADAM17 deficiency led to reduced atherosclerosis development (104). This evidence concerns the gene ADAM17 and atherosclerosis.