Targeting cell adhesion is potentially useful in cancer [31] and exposing BxPC‐3 pancreatic cancer cells that overexpress FXYD3 to a Cysteine‐mutated peptide derivative of full‐length FXYD3 displaces the wild‐type protein, increases doxorubicin‐induced β1 subunit glutathionylation and greatly enhances doxorubicin cytotoxicity. This evidence concerns the gene FXYD3 and pancreatic neoplasm.