Dana‑Farber investigators described a mechanism of resistance to immune checkpoint inhibitors in renal cell carcinoma driven by interferon‑gamma signaling within tumor‑associated myeloid cells. The study maps how IFNγ activity in myeloid populations reprograms the tumor microenvironment to blunt T‑cell activity and therapy response. By pinpointing a cell‑type‑specific signaling axis, the work identifies potential targets for combination strategies to restore checkpoint sensitivity and suggests biomarkers for patient selection in RCC immunotherapy trials.