Redox phenotype confers T cell-exclusion microenvironment and resistance to immunotherapy by suppressing STING/MDA5 expression and interferon signaling in lung cancers harboring KEAP1/STK11 mutations

Collectively, we associated the redox status mediated by loss-function mutations of <i>KEAP1</i> or <i>STK11</i> to immune evasion and immunotherapeutic resistance by suppressing <i>STING</i>/<i>MDA5</i> expression and interferon signaling of cancer cells. Our findings link redox homeostasis to <i>STING/MDA5</i> expression and tumor immunogenicity, raising the possibility that targeting this axis could represent a future strategy to enhance ICI efficacy.