Here, we report that chronic exposure to diesel exhaust particles (DEPs), a major component of PM2.5, induces an immunosuppressive lung microenvironment that promotes tumour progression in a KRAS-driven lung adenocarcinoma model (KrasLSL-G12D/+-Trp53lox/lox or KP mice). The gene discussed is KRAS; the disease is lung adenocarcinoma.