The present study was aimed to shed light on the K+ channel-dependent molecular mechanism of regulation of cell mobility and f-actin dynamics, we provide evidence that KV11.1 is implicated in sustaining pro-metastatic signals in pancreatic cancer, through a reorganization of f-actin in stress fibers and a modulation of filopodia formation and dynamics. The gene discussed is KCNH2; the disease is pancreatic neoplasm.