The breast and ovarian cancer susceptibility genes BRCA1 and BRCA2 are essential for preserving genomic stability, primarily through their role in homologous recombination (HR) repair of DNA double-strand breaks. Consequently, cells harboring germline or somatic mutations in BRCA1 or BRCA2 lack DNA repair via HR and are predisposed to carcinogenesis. Poly (ADP-ribose) polymerase (PARP) inhibitors represent a therapeutic strategy that exploits synthetic lethality in HR-deficient cells. However, PARP inhibition also activates the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, a key regulator of inflammation, and induces expression of the immune checkpoint molecule programmed death-ligand 1 (PD-L1). These effects suggest that immune checkpoint inhibitors (ICIs) may be particularly effective in combination with PARP inhibitors for HR-deficient cancers by counteracting PD-L1-mediated immune evasion. This review examines the molecular mechanisms through which genotoxic stress drives inflammation in HR-deficient cancers and discusses emerging strategies to improve ICI-based immunotherapy by targeting inflammation-associated pathways.