Given that Pfk2 is mis-expressed in tumor cells but not in normal cells (Figure 2a) and that dMyc accumulation is most sensitive to the Pfk2-Pfk mediated committed step of glycolysis specifically in tumor cells (Figure 6), targeting Pfk2 may be a favorable, selective metabolic strategy in the treatment of cancers, especially those displaying ectopic MYC expression. This evidence concerns the gene MYC and neoplasm.