Reduced T-cell priming by Atg16l1 deficient CD8α+ DCs in Ldlr−/− mice fed an HFD could have contributed to the observed decrease of aortic Th1 cells and the reduction of atherosclerosis, given the well-validated proatherogenic role of Th1 immunity.24 However, selective deletion of Atg16l1 in CD8α+ DCs did not reproduce the phenotype. Here, LDLR is linked to atherosclerosis.