We observed that only the ApcMin allele, but not the wild-type allele, was detected in tumors arising from Ifngr1−/−ApcMin/+ mice, as in those from ApcMin/+ mice (Supplementary Figure S3), suggesting that lack of IFN-γ receptor led to increased tumor multiplicity similarly via loss of the wild-type Apc allele. The gene discussed is APC; the disease is neoplasm.