This regulation of cholesterol efflux was specific to the circadian gene Clock and involves the transcription factor USF2, as only Clock knockdown but not the knockdown of Per1, Cry1, or Bmal1 in bone marrow–derived macrophages led to a reduction in Abca1 mRNA levels.117 Given the pivotal role of macrophages in atherosclerosis formation, it was found that Apoe−/− mice receiving bone marrow from ClockΔ19Apoe−/− mice also exhibited more severe atherosclerosis (2–2.7-fold) than those receiving bone marrow from Apoe−/− mice. The gene discussed is CRY1; the disease is atherosclerosis.