KRAS and neoplasm: On a molecular level, this correlated with a strong decrease in the expression of the checkpoint protein CTLA-4, which inhibits T-cell receptor signaling; previous work had shown that induction of MYC in tumor cells induces CTLA4 expression in T-cells in a model of hepatocellular carcinoma, and that CTLA4 increases during tumor progression a KRAS-driven PDAC model53,54.