LGALS3 and hepatocellular carcinoma: Based on the observations that galectin-3 is overexpressed in HCC, and that galectin-3 activates the mTORC1 signaling to regulate the expression of genes that are critically involved in glycolysis, it is reasonable to postulate that galectin-3 promotes glucose uptake and glycolysis through regulating the mTORC1 signaling pathway, leading to the development and/or progression of HCC.