Cytoplasmic tetramer PKM2 severs as a glycolytic enzyme for tumor metabolism, but after translocation into the nucleic, the dimer PKM2 induces nuclear ectopic elaborated as a protein kinase [50, 51], binding to histone H3 and phosphorylates histone H3 at T11 which is responsible for the dissociation of HDAC3 from MYC promoter regions [25]. This evidence concerns the gene WEE1 and neoplasm.