In tumor cells, PKM2 expression is increased by mutually exclusive alternative splicing to favor the inclusion of exon 10 over exon 9 due to oncogene-driven changes in the expression of the splicing factors hnRNPA1/A2 and PTBP1 that suppress exon 9 inclusion, and in the expression of SRSF3, which directs the inclusion of exon 10. This evidence concerns the gene PKM and neoplasm.