The increased extracellular ATP in turn opened the ATP-gated P2 × 7R channel and allowed tumor-derived extracellular cGAMP to reach the cytosol of immune cells to activate the adaptor protein stimulator of interferon genes (STING), which in turn triggered the TANK-binding kinase 1-interferon regulatory factor 3 (TBK1-IRF3)-dependent signaling process, leading to the production of type I IFNs [162,179,180,181,182,183]. The gene discussed is TBK1; the disease is neoplasm.