As PKM gene expression is modulated by c-Myc, STAT3, β-catenin, and HIF1-α, and PKM alternative splicing is under c-Myc control, the kinase activity of PKM2 induces a positive feedback loop that globally enhances the glycolytic phenotype of cancer cells and plays a crucial role in cancer cell metabolism reprogramming [172]. This evidence concerns the gene HIF1A and cancer.