Westphalen and coworkers have explored the tumorigenic potential of DCLK1+ cells in experimental mouse models providing evidence that: (a) the simple introduction of mutant KRas into DCLK1+ cells does not modify the proliferation, survival or longevity of these cells; (b) in contrast, the introduction of a mutant KRAS, together with an inflammatory stimulus (pancreatitis), converts DCLK1+ cells into potent cancer-initiating cells [140]. The gene discussed is DCLK1; the disease is pancreatitis.