Consistent with these findings, growth of ATG16L1-deficient CRC organoids was comparable to that of WT control organoids when implanted orthotopically in the colon mucosa of NSG hosts (Supplementary Fig. 7d, e), in contrast to the defective growth of Atg16l1 KO organoids in immunocompetent BL6 hosts (Supplementary Fig. 7b, c). The gene discussed is ATG16L1; the disease is colorectal carcinoma.