In summary, these data suggest that oncogenic KRAS is a major driver of COX2/PGE2 signaling in mouse and human lung cancer and may therefore contribute to ICB resistance in KRAS-mutant lung adenocarcinoma and tumor relapse in patients treated with KRASG12C inhibitors, which can be overcome by COX2/PGE2 pathway inhibitors. This evidence concerns the gene KRAS and neoplasm.