Given that PKM2 can promote cell proliferation by interaction with a lot of molecules (e.g. histone 1, STAT3, b-catenin) and direct cell differentiation via its interaction with Oct4 [22, 43], it is tempting to assume that PKM2 might function as a key balancer between a hypoxia-promoted growth/survival phenotype and a hypoxia-mediated dedifferentiation phenotype in HCC, both of which need PKM2 high expression to activate numerous transcription factors downstream of HiF1a. This evidence concerns the gene HIF1A and hepatocellular carcinoma.