The ability of STING agonists have the potential to convert ‘cold’ tumors, which lack immune cell infiltration, into ‘hot’ tumors that are more responsive to immunotherapy by promoting the production of chemokines such as CCL5, CXCL9, and CXCL10, which recruit immune cells like T cells and NK cells to the tumor microenvironment, highlights their transformative potential in cancer treatment. This evidence concerns the gene STING1 and neoplasm.