Since the landscape of the tumor/stroma crosstalk FGF/FGFR appeared to play a central role [6,7,8], we very recently demonstrated the specific involvements of the mesenchymal variant of FGFR2 (FGFR2c) and its downstream PKCε aberrant axis in the enhancement of the EMT-profile and the tumorigenic features of PDAC-derived cells [10,11]. The gene discussed is PRKCE; the disease is neoplasm.