AKR1B10 and cholangiocarcinoma: In mechanism, YTHDF2 accelerated degradation of m6A-modified LATS1 mRNA, thus reduced phosphorylation of YAP/TAZ and activated it.223 In addition to these compelling transcription factors (TFs), METTL3 boosted expression of NDUFA4 in GC,224 AKR1B10 in cholangiocarcinoma (CCA),225 NCAPH in clear cell renal cell carcinomas (ccRCC),226 thus promoted glycolysis and malignant phenotypes.