Our studies reported here are potentially in conflict with the recently published work of Heeschen and colleagues [65, 66]. In their work, the authors report that ectopic mir-17~92 expression promotes the proliferation of pancreatic cancer stem cells, resulting in their premature depletion and consequent reduced cell transformation and tumorigenicity. In contrast, our studies demonstrate that ectopic mir-17~92 increases MEK/ERK signaling, a feature required for the maintenance of established PanIN lesions [6, 67], suggesting that elevated mir-17~92 levels should enhance pancreatic cancer development. However, we have not evaluated the self-renewal capacity of mir-17~92 expressing PanIN cell lines, nor have we tested their tumorigenic capacity upon implantation into recipient mice. Future experiments in genetically engineered PDAC mouse models with enhanced mir-17~92 expression may be required to resolve this discrepancy.