In contrast, M2 macrophages are essential for tissue repair and resolution of inflammation, leading to symptom alleviation.[48] Polarization of macrophages toward the M1 phenotype has been strongly implicated in IBD pathogenesis, while therapies targeting TNF‐α have been successful in reducing disease severity by shifting macrophage polarization toward the M2 phenotype.[49] Thus, modulation of macrophage polarization is increasingly recognized as a promising therapeutic approach in IBD. The gene discussed is TNF; the disease is inflammatory bowel disease.