For example, KRAS is mutated in nearly 95% of all pancreatic ductal adenocarcinoma (PDAC) patients, a particularly aggressive and deadly form of cancer (2, 3), where it has been shown to potently activate extracellular signal–regulated kinase 1/2 (ERK1/2) and PI3K and give rise to enhanced cell growth, chemoresistance, migration, and invasion, as well as metastatic spread. Here, MAPK3 is linked to cancer.