These two isoforms result from alternative splicing of the PKM transcript, and this splicing is controlled by the hnRNP family (hnRNPA1, hnRNPA2 and PTB), which repressively binds the sequences flanking exon 9 and promotes the formation of PKM2.[12, 23, 24] C-Myc up-regulates transcription of hnRNP family proteins and increases the PKM2/PKM1 ratio in many cancers.[12] Here, we demonstrate that hnRNPA1 contributes to the generation of PKM2 but inhibits PKM1 production in glioma cells. Here, PKM is linked to central nervous system cancer.