We evaluate three interconnected themes: disease mechanisms, where dysregulated m6A drives oncogenesis (e.g., METTL3‐mediated hypermethylation in breast cancer) and contributes to neuropsychiatric/cardiovascular disorders; homeostatic functions, spanning embryogenesis (maternal‐to‐zygotic transition), tissue regeneration (YTHDF1 in muscle), and immune regulation; therapeutic frontiers, including enzyme‐targeting strategies (FTO inhibitors, METTL3 stabilizers) and diagnostic approaches. This evidence concerns the gene FTO and breast cancer.