Previous studies have reported that ALDOA was a critical driver for HCC cell growth under hypoxia, and considered as a promising therapeutic strategy for treating HCC30,31, and a study using paired tumor and adjacent liver tissues of hepatitis B virus-related HCC patients revealed that phosphorylation of glycolytic enzymes including ALDOA might drive metabolic reprogramming and proliferation in beta-catenin-mutated HCC32. Here, CTNNB1 is linked to neoplasm.