Compared to WT control hosts (Fig. 2d), loss of host IFNγ significantly increased liver colonization by Atg16l1 KO CRC organoids as shown by BLI quantification (Fig. 2g, h; Supplementary Fig. 8d; WT host vs. IFNγ KO host), macroscopic tumor nodule count (Supplementary Fig. 8e), and histologic examination (Supplementary Fig. 8f, g), suggesting that host IFNγ suppresses the growth of ATG16L1-deficient CRC organoids in vivo. The gene discussed is ATG16L1; the disease is neoplasm.