KRAS and neoplasm: In addition, Briere et al. (7) using the same model demonstrated a switch in the tumor microenvironment (TME) from immunosuppressive in the vehicle setting, with high presence of M2 macrophages and myeloid-derived suppressor cells, to favoring antitumoral immune response following KRAS-G12C inhibition with adagrasib, another clinically approved KRAS-targeted drug.