Nonetheless, many of the genetic alterations that occur in cancer uncouple MYC expression from these usual regulatory constraints: either constitutive activation of signal transduction pathways (e.g., Notch, Wnt and receptor TKs) or direct alterations of MYC, such as point mutations, leading to protein stabilization, amplifications or translocations[37,44], can lead to its deregulation. This evidence concerns the gene MYC and cancer.