An overexpression of gal-3 in pancreatic tumor tissue contributes to PDAC progression via gal-3 binding to retaining Ras at the plasma membrane maintaining Ras-signaling including phosphorylation of Extracellular-signal Regulated Kinases (ERK) and AKT and Ras-like (Ral) protein A activity (12–14). Here, LGALS3 is linked to pancreatic neoplasm.