CGAS and neoplasm: Tumor cells frequently harbor genomic instability, sustain DNA damage, and endure cell cycle dysregulation and mitochondrial stress, accumulating free cytosolic dsDNA to trigger cGAS activation(Crasta et al., 2012; Riley et al., 2018), thus initiating a potent IFN-dependent innate immune response and recruiting cytotoxic effectors to mount antitumor immunity(Gao et al., 2013; Khoo and Chen, 2018; Lam et al., 2014; Marcus et al., 2018), mainly through helper T lymphocytes and natural killer cells.