The reversibility of butyrophilin-like1 (Btnl1)-deficience in mice suggested cancer cells thrive in the absence of Vγ7+ cells, which play the pivotal role of human and mouse intraepithelial lymphocytes (IELs) expressing γδ T-cell receptors (γδTCRs) in cancer immunosurveillance. In this study, β-catenin signaling in IECs decreased expression of Btnl genes and the transcription factors that regulate them, HNF4A and HNF4G. This molecular rewiring also promoted γδ T-cell exclusion from tumors. And, the inhibition of β-catenin signaling via genetic deletion of Bcl9/Bcl9l in either Apc-deficient or mutant β-catenin mouse models restored Hnf4a, Hnf4g, and Btnl gene expression and γδ T-cell infiltration into tumors. These observations highlight an immune-evasion mechanism specific to WNT-driven colon cancer cells that disrupts γδIEL immunosurveillance and furthers cancer progression.