In accordance with the Clock mutant data discussed above, global deficiency of BMAL1 as seen in double-deficient Apoe−/−Bmal1−/− and Ldr−/−Bmal1−/− mice accelerated atherosclerosis (2–7-fold) and promoted macrophage infiltration (≈4-fold) in lesions.116 Similarly, hepatocyte specific Bmal1 (AlbCre:Bmal1flox) deficiency in Apoe−/− mice116 and vascular SMC-specific Bmal1 (SmmhccreERT2:Bmal1flox) deficiency in western diet-fed mice39 also promoted atherosclerosis (≈2-fold) and monocyte transendothelial migration39 (Table 2). This evidence concerns the gene BMAL1 and atherosclerosis.