The mechanism underlying PARPi efficacy is still under investigation [34, 35] Indeed, beside the synthetic lethality in HR (homologous recombination)-deficient tumor cells, PARPi have been considered to exert their anti-tumor activity also by recruiting CD8 + T lymphocytes via STING pathway enhancing anti-tumor immune response by increasing the production of IFN-y, regardless of BRCAness [34]. The gene discussed is STING1; the disease is neoplasm.