Studies conducted in genetically engineered murine models exhibiting spontaneous tumors driven by mutated KRAS have demonstrated that oncogenic KRAS orchestrates an immunosuppressive TME [86, 87] In these models, KRAS activation leads to increased secretion of IL23, CCL9, VEGFA, and CXCL3 by tumor cells, which recruit immunosuppressive macrophages and myeloid-derived suppressor cells (MDSCs) into the TME, resulting in the exclusion of adaptive T and B cells in a PD-L1–dependent manner. This evidence concerns the gene KRAS and neoplasm.