STING1 and neoplasm: Following cellular stimulation by external factors such as tumor-derived DNA, intracellular cGAS protein becomes activated, triggering the translocation of STING protein from the endoplasmic reticulum (ER) to the Golgi apparatus, where it undergoes phosphorylation and subsequently activates downstream p-TBK and p-IRF3, ultimately leading to interferon signaling transcription [27].