Pancreatic Ductal Adenocarcinoma (PDAC) still represents a therapeutic dead-end. The
inventors report that the K+ channel SK2 is stimulated by secreted cues from cancer-associated fibroblasts (CAF) leading to the activation of an Integrin-EGFR-AKT signaling axis which
participates to the acquisition of pro-metastatic features. The inventors show that SK2 acts as a pivotal signaling regulator as being both a direct target of AKT and an amplifier of AKT downstream transduction. The present invention relates to a method of treatment of pancreatic
cancer in a patient in need thereof comprising a therapeutically effective amount of SK2
inhibitor.