While m6A's regulatory impact on macrophage function has been reported, its effects are context‐dependent, varying under different physiological conditions.[12, 13, 14] For example, m6A modification of Socs1 suppresses macrophage inflammation during bacterial infections,[14] whereas m6A modification of Irakm enhances macrophage activation in response to TLR4 ligands.[13] These studies have primarily focused on the TLR4 signaling pathway in macrophages, but the role of m6A in regulating macrophage polarization through TLR7 signaling remains poorly understood. This evidence concerns the gene SOCS1 and bacterial infectious disease.