Consistent with its roles in oncogenesis, MYC is frequently overexpressed in human cancers via various mechanisms, including gene amplification, chromosomal translocation, increased MYC translation, deregulated MYC protein stabilization, or constitutive activation of upstream pathways such as Wnt, Notch, Hedgehog signaling (Nesbit et al., 1999; Dang, 2012b; Kress et al., 2015). The gene discussed is MYC; the disease is cancer.