Mechanistically, m6A may dictate the fate of tumor suppressor or oncogenic transcripts (e.g., BCL2, BNIP3, c-MYC, CXCR4, and CYP1B1), influence the treatment outcomes (e.g., resistance to tamoxifen or doxorubicin via methylation of AK4 or miRNA-221–3p) or regulate the stability of pluripotency factors (e.g., Nanog and KLF4), thus facilitating epithelial-mesenchymal transition (EMT), metastatic progression or the breast cancer stem cell phenotype, among others. The gene discussed is MYC; the disease is breast carcinoma.