Previous reports have shown that ligand-independent EphA2 signaling (pS897-EphA2) induced by RSK1/2 and/or AKT signaling is a trigger for pancreatic cancer chemoresistance, and the N-terminal truncated EphA2 fragment can be a transmitter at the cancer cell surface for pS897-EphA2 signaling (7, 37). This evidence concerns the gene EPHA2 and pancreatic neoplasm.