The theoretical basis for the combined use of PARP inhibitors and immunotherapy is mainly based on two assumptions: first, PARP inhibitors can increase tumor mutation burden and thereby increase the production of new antigens, stimulating anti-tumor immune response when treating HRD tumors; second, PARP inhibitors can activate innate immune responses by activating the STING pathway and upregulating PD-L1 expression, thus enhancing anti-tumor effects (121). This evidence concerns the gene STING1 and neoplasm.