Indeed, whether resulting from direct alterations of the locus (e.g., gene amplification, translocation) or from the activation of upstream signaling pathways (receptor tyrosine kinases, Ras, Raf, Wnt, Notch, etc.), most tumor types show deregulated MYC expression, resulting in uncontrolled activation of MYC‐driven programs. This evidence concerns the gene MYC and neoplasm.