Furthermore, downregulation of PKM2 by siRNA treatment caused cell cycle arrest at G0/G1 phase in bladder cancer cells, which is supported by previous studies showing that dimeric PKM2 enhances cellular biosynthesis and expression of cyclin D1 by upregulating the expression of c-Myc and promoting nuclear translocation of β-catenin [38], and PKM2 directly phosphorylates histone H3 at T11, resulting in H3-K9 acetylation and transcription of genes, including CCND1 [39]. This evidence concerns the gene MYC and urinary bladder cancer.