The preferential expression of Pyruvate kinase isozyme M2 (PKM2) is related to increased aerobic glycolysis and the growth advantage of cancer cells.45 After the depletion of DNA methyltransferase three beta (DNMT3β) or Brother of the Regulator of Imprinted Sites (BORIS) and the mutation of Bardet–Biedl syndrome (BBS) at exon 10 of PKM, the splicing transition from PKM2 to PKM1 isomer is related to the reversal of the Warburg effect, which further inhibits the growth of breast cancer cells. The gene discussed is DNMT3B; the disease is breast cancer.