Researchers at Dana‑Farber Cancer Institute identified interferon‑gamma (IFNγ) signaling within tumor‑associated myeloid cells as a mechanism driving resistance to immune checkpoint inhibitors (ICIs) in renal cell carcinoma. The study mapped myeloid cell signaling programs and showed how chronic IFNγ activation in these cells reshapes the tumor microenvironment to blunt T‑cell mediated clearance, according to the Dana‑Farber report. The work nominates myeloid IFNγ pathways as therapeutic targets to overcome ICI resistance and suggests combinatorial approaches—myeloid‑directed agents plus checkpoint blockade—could restore sensitivity. The paper highlights how dissecting non‑tumor cell compartments can reveal actionable resistance mechanisms.