It has been reported that METTL3 mediates m6A modification to participate in the mRNA transcription of IL-6, which would promote the deacetylation of METTL3 at K177 site, and subsequently deacetylated METTL3 is able to enter the nucleus, mediate nuclear translocation, induce global m6A abundance, and thus induce metastasis of BC. This evidence concerns the gene IL6 and breast cancer.