Recently, Sebti’s group also revealed a link between CDK hyperactivation and mutant Kras dependency through comparative phosphoproteomics and CRISPR/Cas9 gene editing, and consequently found that knocking out the CDK1, 2, 7, and 9 was as effective as knocking out Kras in mutant Kras-driven pancreatic cancer.11 Here, KRAS is linked to pancreatic neoplasm.