In view of their crucial role in cancer cell viability, it is conceivable that downregulation of Na +/K+-ATPase subunits and hampering of PI3K/AKT/GSK3β/β-catenin pathway contribute to cell growth inhibition, viability and clonogenicity impairment, as well as cell death induction in pancreatic cancer cells treated with nitroxoline, which we observed both in the present and in a previous study7. This evidence concerns the gene GSK3B and pancreatic neoplasm.