Although it is difficult to reconcile the findings from this single discordant report with those of the other two studies as well as the present study, we believe that the combined use of recombinant protein analyses, cell lines derived from several types of cancer, two methods to inhibit PFKFB4 (siRNA and genomic deletion) and PFKFB4 over-expression experiments provide comprehensive and compelling data demonstrating that the kinase activity of PFKFB4 dictates the F2,6BP concentration in transformed cells. Here, PFKFB4 is linked to cancer.