Loss of cGAS or STING results in impaired senescence and SASP responses, leading to accelerated spontaneous immortalization and increased tumor growth.182,184–186 Interestingly, cGAS can also intervene in cell replication in a STING-independent manner, acting as a “brake” to suppress genomic instability.199 Contradictorily, nuclear-localized cGAS has been shown to inhibit homologous recombination repair (HRR) of damaged DNA, thereby promoting tumorigenesis.200 However, these two findings offer different implications for cGAS at different stages of tumor development. This evidence concerns the gene STING1 and neoplasm.