STAT3 and gastric cancer: Likewise, Kim et al. reported that WNT1 overexpression in gastric cancer cells upregulates p-STAT3 (Y705) and p-STAT3 (Y705) nuclear accumulation in a β-catenin-dependent manner and further proved that galectin-3 is responsible for bridging the WNT/β-catenin and STAT3 signaling pathways, culminating in gastric tumor progression [58].