The primary means by which APC inactivation contributes to colon adenoma and CRC development is believed to be the resultant dysregulation in the levels and localization of the β-catenin protein, particularly the role of nuclear β-catenin as a binding partner for the T cell factor (TCF) family of transcription factors and the function of β-catenin/TCF complexes as key regulators of the expression of certain genes [1]. The gene discussed is HNF4A; the disease is colon adenoma.