Increased clearance of Atg16l1 KO tumors by cytotoxic lymphocytes and IFNγ (Fig. 2), along with a persistently enhanced IFN-response gene signature in NSG mice (Fig. 3) prompted us to directly characterize the role of tumor-intrinsic ATG16L1 in regulating IFNγ signaling. The gene discussed is IFNA1; the disease is neoplasm.