Taken together, our results suggest that most SMC phenotypes in advanced atherosclerotic lesions are conserved between humans and mice, and, taken with previous knowledge that SMCKlf4 is atheropromoting in mice and contains a human GWAS CAD risk locus, help us to infer that Klf4-dependent changes in SMC phenotype to an Lgals3+ state are likely detrimental for atherosclerosis pathogenesis. The gene discussed is KLF4; the disease is atherosclerosis.