In BRCA1-deficient ovarian cancer cells, PARP1 inhibited antitumor immunity, whereas the inhibition of ADP-ribosylation increased the infiltration of antigen-presenting cells (including CD45+CD11b+MHCII+ macrophages characterized by pTBK1 and pIRF3) to pathological sites and led to STING-dependent increases in IFN-β and CXCL10 [82]. This evidence concerns the gene PARP1 and ovarian carcinoma.