METTL3 facilitated the proliferation of BC through -acceleration of maturation of pri-miR 221/222 in an m6A-dependent manner to decrease PTEN expression, and METTL3 was also capable of modulating the AFF4/NF-κB/MYC signaling pathway in an m6A-dependent manner, giving rise to progression of BC [17]. This evidence concerns the gene MYC and breast cancer.