The key proviso, of course, is absence of toxicity, which may be more likely for co-targeting the upstream oncogenic activator (not active in normal cells, e.g., BRAV600E) in combination with a downstream effector (functional in both normal and tumor cells, e.g., c-Myc [Soucek et al., 2008]) at optimized drug concentrations. The gene discussed is MYC; the disease is neoplasm.