In patients with defective Excision Repair Cross-Complementation Group 1 (ERCC1), a particular homologous repair deficiency, with non-small cell lung cancer (NSCLC), PARPi therapy created cytoplasmic chromatin fragments that triggered cGAS/STING to produce type I IFNs and CCL5 [58]. This evidence concerns the gene STING1 and non-small cell lung carcinoma.