A positive feedback mechanism was suggested in the progression of breast cancer, where upregulated METTL3 promoted the expression of hepatitis B X-interacting protein (HBXIP) in an m6A-dependent manner, and HBXIP inhibited miRNA let-7 g, a METTL3 negative regulator, thereby maintaining the high expression level of METTL3 and the accelerated cell proliferation in breast cancer [63]. The gene discussed is METTL3; the disease is breast carcinoma.