Studies in pancreatic cancer cell lines additionally demonstrated roles for the mir-17~92 cluster in PDAC cell proliferation, transformation and invasion [25, 38, 39]. However, to date no studies have been performed to evaluate the role of the cluster in vivo during pancreatic tumor initiation and progression. Given the upregulation of these miRNAs in human pancreatic cancers and their validated role as oncogenes in a variety of contexts, we hypothesized that they contribute to KRAS-induced pancreatic tumorigenesis. Therefore, we experimentally tested the requirement for mir-17~92 in a mouse model of pancreatic cancer.