In particular, it has been observed that down-regulation of MBD2 and/or p66α, which triggered derepression of epithelial regulators via epigenetic reprogramming of the Mi-2/NuRD CRC into the MBD2-free or disentangled CRC, resulted in promoted epithelial differentiation and loss of tumor-initiating ability. This evidence concerns the gene MBD2 and neoplasm.