Both EGFR and EpCAM are known downstream target of β‐catenin in HCC.[21, 22] Their overexpression facilitated the acquisition of tumor aggressiveness, resistance, and cancer stem features and strongly correlated with poor patient survival.[43, 44] We additionally show that NR2E3 depletion in human cancer cells increased cell proliferation, migration and invasion capacity, tumor sphere formation, and xenografted tumor formation associated with enhanced β‐catenin signaling activation. This evidence concerns the gene EPCAM and hepatocellular carcinoma.