Taken together, our results indicate that loss of Klf4 in SMC is associated with marked decreases in lesion SMCs that exhibit an Lgals3+ osteogenic phenotype, which is of major interest given our previous studies in SMC Klf4 knockout mice that show loss of Lgals3-expressing SMC as well as decreased lesion size and increased fibrous cap thickness.3 Together with our finding that SMCKlf4 may regulate genes involved in genetic risk for CAD, this implies that Lgal3+ SMCs have negative implications for atherosclerosis pathogenesis. This evidence concerns the gene KLF4 and atherosclerosis.