Evidence has been gathered to suggest that inhibiting Myc markedly impedes tumor progression and cell survival regardless of its normal or dysregulated state in tumors.246,252,253 Moreover, despite the fact that c-Myc is widely expressed in normal proliferating cells, in vivo studies have demonstrated that long-term and whole-body genetic silencing of c-Myc resulted in remarkably mild and reversible side effects.254–256 Together, these findings indicate that the pursuit of modulators of the c-Myc/Max interaction offer a viable and promising anticancer therapeutic target. The gene discussed is MYC; the disease is neoplasm.