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The efficacy of current first\u2010line treatment is dismal, and novel agents are urgently needed to improve patient outcomes. A close association between the cyclic GMP\u2010AMP synthase\u2010stimulator of interferon genes (cGAS\u2010STING) pathway and tumor promotion exists, revealing prospective therapeutic targets. This study, investigates the role of the cGAS\u2010STING pathway and its underlying mechanisms in PTCL progression. Single\u2010cell RNA sequencing showes that the cGAS\u2010STING pathway is highly expressed and closely associated with PTCL proliferation. cGAS inhibition suppresses tumor growth and impaires DNA damage repair. Moreover, Cdc2\u2010like kinase 1 (CLK1) is critical for residual tumor cell survival after treatment with cGAS inhibitors, and CLK1 suppression enhances sensitivity to cGAS inhibitors. Single\u2010cell dynamic transcriptomic analysis indicates reduced proliferation\u2010associated nascent RNAs as the underlying mechanism. In first\u2010line therapy, chemotherapy\u2010triggered DNA damage activates the cGAS\u2010STING pathway, and cGAS inhibitors can synergize with chemotherapeutic agents to kill tumors. The cGAS\u2010STING pathway is oncogenic in PTCL, whereas targeting cGAS suppresses tumor growth, and CLK1 may be a sensitivity indicator for cGAS inhibitors. 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