METTL14 and obesity due to melanocortin 4 receptor deficiency: The dynamic installation and removal of m6A are orchestrated by a tripartite enzymatic network: methyltransferase dimers, primarily METTL3 (methyltransferase-like 3) and METTL14 (methyltransferase-like 14), serve as “writers”; the demethylases FTO (fat mass and obesity-associated protein) and ALKBH5 (alkB homolog 5) act as “erasers”; and “reader” proteins, notably those containing YTH domains, interpret the methyl mark to direct downstream outcomes [4].