METTL3 and neoplasm: The deep sequencing of m6A and mRNA showed that the knockdown of METTL3 and/or METTL14 led to the upregulation of oncogenes and genes coding downstream proteins, including ADAM metallopeptidase domain 19 (ADAM19), EPH receptor A3 (EPHA3), Kruppel-like factor 4 (KLF4) and tumour-inhibiting factors, resulting in the inhibition of GSC growth and self-renewal [85].