In the “KPC” genetically engineered mouse model of PDAC (in which mutant Kras and p53 are targeted for expression in the pancreas, resulting in a high fidelity model of the disease), there is no anti-tumor response in spontaneous tumors to single (CTLA-4, PD-1, PD-L1) or combination (CTLA-4 plus PD-1/PD-L1) immune checkpoint blockade (7, 8). Here, KRAS is linked to neoplasm.