Previous studies have consistently reported that PARP inhibitor can activate the cGAS‐STING pathway, downstream type I IFN signaling and CCL5 secretion in NSCLC due to the induction of DNA repair deficiencies in cancer cells.[36, 37] Although we previously find that KMT5C plays an important role in promoting liver tumor progression by activating DDR, and that KMT5C inhibition can enhance the efficacy of PARP inhibitor in liver cancer,[16] its role in the regulation of tumor immunity has not been unexplored. This evidence concerns the gene CCL5 and non-small cell lung carcinoma.