In order to evade this DNA detection pathway to survive, there are several mechanisms utilized by tumor cells, yielding the defective cGAS-STING signaling in tumors, including decreased the protein level of STING and cGAS, hypermethylation of CGAS and STING1 promoter regions, and defective STING translocation to the Golgi where it normally signals (Khoo and Chen, 2018). The gene discussed is STING1; the disease is neoplasm.