Because such effects might be subtle for any individual gene, and because “master regulators” of the transcriptional response are often not transcriptionally regulated themselves, we tested our hypothesis by computationally searching for connections between human atherosclerosis/CAD risk-associated single nucleotide polymorphisms (SNPs) and monocyte eQTLs for orthologs of genes that are differentially expressed in plaque CD68+ cells in response to lipid lowering (as had been previously applied to a transcriptome study of whole aortic arches [30]). Here, CD68 is linked to atherosclerosis.