Specifically, loss of the tumor suppressor STK11/LKB1 in the presence of a KRAS mutation promotes IL-6–mediated neutrophil recruitment, limits CD8+ T-cell infiltration, and upregulates exhaustion markers such as PD-1, CTLA-4, and TIM-3, collectively generating an ‘immune-cold’ tumor microenvironment and conferring resistance to PD-1/PD-L1 blockade (53–55). The gene discussed is HAVCR2; the disease is neoplasm.