Xie et al. found that the depletion of aberrantly expressed YTHDF2 could suppress the capability of mRNA degradation (including tumor suppressor SETD7 and KLF4) and impede cell migration in vivo and in vitro via recognition of METTL3-catalyzed sites, which suggest that the important role of YTHDF2 in progression of BC may work through METTL3/ YTHDF2/SETD7/KLF4 m6A axis [39]. The gene discussed is KLF4; the disease is breast cancer.