Recent studies have shown that, under conditions such as genomic instability, mitochondrial damage, epigenetic dysregulation, and therapy-induced stress, lung cancer cells can release a variety of abnormal DNA, RNA, and damage-associated molecular patterns (DAMPs), thereby activating key innate immune pathways, including cGAS-STING, Toll-like receptor (TLR), and RIG-I-like receptor (RLR) signaling. Here, CGAS is linked to lung carcinoma.