Although the relative requirement of the kinase versus the bisphosphatase domain for cancer cell survival has been somewhat controversial [14-16], recent studies have demonstrated that: (i) recombinant human PFKFB4 kinase activity is 4.3-fold greater than its phosphatase activity; (ii) both PFKFB4-specific siRNA and genomic deletion of Pfkfb4 result in a decrease in the steady-state concentration of intracellular F2,6BP (the product of the kinase domain); and (iii) over-expression of PFKFB4 increases F2,6BP in vitro [16]. This evidence concerns the gene PFKFB4 and cancer.