Restoring IFN activity via STING agonists or IFN-β administration reverses immunosuppressive microenvironments by converting “cold” to “hot” tumor phenotypes, enhances B/NK cell infiltration, and synergizes with PD-1/PD-L1 blockade, demonstrating improved prognosis in preclinical models (122, 123). This evidence concerns the gene IFNA1 and neoplasm.