Taken together with the present findings, these observations suggest that PDAC may be “primed” to exhibit increased DUSP1 activation in response to gemcitabine, and suggest that targeting DUSP1 in PDAC could enhance the beneficial actions of gemcitabine by promoting apoptosis and suppressing pancreatic cancer cell proliferation and tumor angiogenesis. Here, DUSP1 is linked to pancreatic neoplasm.