Based on this phenotype, as well as the synthetic lethality between POLθ inhibition and HR-deficiency, and recent data demonstrating activation of the cGAS/STING pathway upon combined knockout of POLQ and FANCD2 in esophageal cancers18, we hypothesized that POLθ inhibition in BRCA-deficient cancers would likewise activate the cGAS/STING pathway and lead to increased T-cell infiltration and activation, with sensitization to immune checkpoint blockade. The gene discussed is STING1; the disease is cancer.