For instance, RAS mutation was shown to contribute to the oncogenic role of N-Myc.50 The tyrosine kinase SRC has also been implicated in mediating growth factor signal-induced C-Myc expression.51,52 Even though a complex scenario likely exists for generation of superfluous protein requiring degradation—with Myc being a player—we can speculate that tumours would be primed to HDAC6 inhibitors as demonstrated in this report.53 This evidence concerns the gene MYCN and neoplasm.