To evade this DNA detection pathway to survive, there are several mechanisms used by tumour cells to generate defective cGAS-STING signalling, including reductions in the protein levels of cGAS and STING, hypermethylation of cGAS and STING promoter regions, and defects in STING translocation to the Golgi body, its usual signalling site [49, 50]. The gene discussed is STING1; the disease is neoplasm.