EGFR and neoplasm: 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.