Consistently, the expanded aortic Tregs in vivo, limited accumulation of Th1, and reduced development of atherosclerosis in CD11cCre−Atg16l1flox/floxLdlr−/− mice (Atg16l1 deletion in total DCs) were proven to be caused by CD11b+DC subset, as no such effects were seen when Atg16l1 was deleted selectively in conventional CD8a+DCs and CD103+DCs (63). This evidence concerns the gene ITGAM and atherosclerosis.