Background: A subset of metastatic melanoma patients shows evidence for a T cell-inflamed tumor microenvironment at baseline, which has prognostic value and is associated with clinical response to immunotherapies including anti-PD-1. However, the molecular mechanisms mediating the absence of T cell infiltration in a major subset of patients have not been defined. Methods: Exome sequencing and gene expression profiling of melanoma metastases (TCGA) was combined with mechanistic studies in genetically engineered mouse models. Results: Analysis of melanoma metastases samples using gene expression profiling and exome sequencing, revealed activation of Wnt/ß-catenin pathway in a major subset of non-T cell-inflamed tumors. Using genetically engineered mouse melanoma models (Braf^V600E/PTEN^-/-± active ß-catenin), we demonstrated a causal effect between tumor-intrinsic ß-catenin signaling and T cell exclusion from the tumor microenvironment. The mechanism was via failed production of the chemokine CCL4, which was associated with failed recruitment of Batf3-lineage dendritic cells. Mice with these non-T cell-inflamed melanomas failed to respond to anti-CTLA-4/anti-PD-L1 mAb therapy. Active Wnt/ß-catenin signature in human melanomas was associated with reduction of Batf3 dendritic cell transcripts. Clinically, a patient who responded to a melanoma vaccine then recurred showed selection for loss of the T cell signature and gain of the ß-catenin phenotype. Conclusions: We have for the first time identified an oncogenic pathway that directly mediates immune evasion, which is implicated in examples of both primary and acquired resistance to immunotherapies.