The study in Ldlr−/− mice found that Atg16l1-deficient CD11b+ DCs produced a TGF-β-dependent tolerance phenotype and promoted CD4+ Treg cell expansion, reducing the development of atherosclerosis.117 Recent studies have reported that Alisol B 23-acetate (23B), a new promoter for cholesterol efflux in DCs, alleviates inflammation and dyslipidemia in advanced atherosclerosis of mice, thereby controlling the atherosclerotic inflammatory state.118 These findings expand our understanding of how DCs affect atherosclerosis and provide new potential approaches to prevent atherosclerosis. The gene discussed is ATG16L1; the disease is atherosclerosis.