YTHDC1 and neoplasm: The recently identified NAT10/ac4C-YTHDC1/m6A-LDHA/PFKM signaling axis promotes glycolysis in osteosarcoma (OS) cells by a unique mechanism: NAT10-mediated ac4C modification suppresses the expression of the m6A reader YTHDC1, which in turn reduces the m6A methylation and stability of key glycolytic enzymes LDHA and PFKM mRNAs, ultimately enhancing glycolytic flux and supporting tumor progression [333].