Coordination of c-Myc with cyclin D1 or its upstream activators may not only accelerate tumor formation but also drive tumor progression to a more aggressive phenotype. Because c-Myc may affect immortalization while cyclin D1 elicits transformation, agents that target c-Myc and cyclin D1 can be good chemopreventive agents [11]. Recently, c-Myc has been recognized as an important regulator of stem cell biology as it may serve as a link connecting malignancy and “stemness” and has central role in cell proliferation, apoptosis, and survival of CSCs [12–14]. CD133-positive colon CSCs were shown to be resistant to the conventional cytotoxic drug FU and the resistance was shown recently to be dependent on Wnt signaling [15].