This abnormal accumulation of c-Myc in human cancers can be attributed to multiple causes, for instance, gene translocation and amplification [2,4,40,41,43,44], gene mutations on hot spots, e.g., Thr58 which abolishes c-Myc phosphorylation and results in decreased ubiquitination and proteasome-mediated degradation of c-Myc [7,18,19], and dysregulation of the mechanistic signaling pathway controlling c-Myc stability. Here, MYC is linked to cancer.