Their core strength lies in reprogramming the immunosuppressive tumor microenvironment (TME): IONPs polarize M2-polarized tumor-associated macrophages (TAMs) to antitumor M1 phenotypes, activate innate immune pathways like STING, and induce immunogenic ferroptosis, converting “immune-cold” tumors into inflamed, treatment-responsive states. The gene discussed is STING1; the disease is neoplasm.