KRAS and neoplasm: However, despite intensive efforts, strategies to target KRAS have been limited by the lack of a proper binding pocket for small molecules, and no applicable targeted strategy directly targeting KRAS itself or its downstream effectors has been approved for clinical use.45,46 A growing body of evidence implies that KRAS-driven malignancies are associated with extensive stromal remodeling which may be alternatively targeted to prevent tumor progression.47,48 In agreement, we here demonstrated that mutant KRAS induces an immune-suppressive microenvironment that favors tumor progression.