These include exploiting synthetic lethality—for example, targeting BRCA-deficient tumors with PARPi (Tiek and Cheng, 2022); dual inhibition of compensatory signaling pathways, such as co-targeting hormone receptors and cell cycle regulators (Shieh, 2022); and activating anti-tumor immunity—for instance, PARP inhibition can trigger the cGAS/STING pathway and upregulate PD-L1 expression, thereby enhancing CD8+ T-cell infiltration. The gene discussed is PARP1; the disease is neoplasm.