FOXA2 and cancer: NEF, transcriptionally activated by FOXA2, physically interacts with β-catenin to increase GSK3β–β-catenin binding and thus promoting the inhibitory phosphorylation of β-catenin, resulting in FOXA2 upregulation and inhibited Wnt/β-catenin signaling, eventually suppressing EMT progression and cancer metastasis [53].