More than 85% of KEAP1-mutant non–small cell lung cancer (NSCLC) patients display primary resistance to immune checkpoint inhibitors (ICIs), yet the tumor-intrinsic mechanisms driving immune escape remain poorly defined. Here, we uncover a previously unrecognized role of KEAP1 in promoting antitumor immunity by targeting CARMA3 for ubiquitin-mediated degradation, thereby restraining activation of the non-hematopoietic CARMA3–BCL10–MALT1 (C3BM) signalosome. Loss of KEAP1 stabilizes CARMA3, triggering aberrant C3BM activation and chronic NFkB signaling. This sustained pathway activation drives the release of pro-tumorigenic chemokines, including CCL2 and CXCL1, which remodel the tumor microenvironment into an immunosuppressed niche that facilitates immune evasion. Genetic or pharmacologic disruption of C3BM signaling—through CARMA3 depletion, MALT1 inhibition, or chemokine receptor blockade—restores innate and adaptive antitumor immunity, suppresses KEAP1-mutant tumor growth, and sensitizes tumors to ICIs. Together, these findings establish C3BM signaling as a tumor-intrinsic driver of immune escape in KEAP1-mutant NSCLC and define a therapeutically actionable pathway to overcome immunotherapy resistance.