It has been reported that inactivation of GSK-3β, one of the key components of the β-catenin degradation complex, via the PI3K-Akt signalling pathway causes β-catenin dephosphorylation and nuclear accumulation in colon cancer.27 Enrichment analysis (Fig. 2a) showed that Galectin-3 was significantly correlated with the PI3K-Akt signalling pathway; therefore, we explored whether PI3K-Akt signalling-mediated GSK-3β inactivation was involved in Galectin-3-induced β-catenin nuclear translocation in HCC cells. The gene discussed is AKT1; the disease is hepatocellular carcinoma.