Excess Myc expression can be induced upon retroviral promoter insertion, chromosomal translocation/amplification, activation of super-enhancers within the MYC gene, and/or mutation of upstream signaling pathways that enhance Myc stability.5 Studies in transgenic mouse models have demonstrated that even transient inactivation of Myc elicits tumor regression, suggesting that regulation of oncogenic Myc could be harnessed to treat cancer patients.8–10 Yet, drug development aimed at directly targeting Myc has proved challenging. The gene discussed is MYC; the disease is cancer.