Mice that lack BECLIN1 or RB1CC1, but not ATG5, ATG16L1, and ATG7, in myeloid cells also display spontaneous immune activation and resistance to Listeria infection [65] whereas ATG16L1 promotes plasma membrane repair to limit Listeria spread independent of other autophagy proteins [66], indicating that individual autophagy proteins or complexes have functions in countering inflammation that cannot be explained by autophagosome-dependent pathways. This evidence concerns the gene ATG16L1 and listeriosis.