We read with great interest the recent report of Zhao et al.1 The authors have provided experimental evidence that shows the effect of exogenous galectin-3 (GAL3) on pancreatic stellate cell (PSC) activation and its consequence on the pancreatic ductal adenocarcinoma (PDAC) growth.1 The presence of a high number of activated PSCs or cancer-associated fibroblasts (CAFs) in PDAC tissues is a hallmark of this disease.2 The molecular crosstalk between PDAC cells and PSCs are known to cooperatively promote cancer progression.