Our experiments were initiated with the idea of establishing the mechanistic basis of the anti-M2 effects of TNF; in part, we reasoned that as anti-TNF biologics have a vast spectrum of activities in RA and IBD patients, we should be able to elucidate a signaling framework that connects successful anti-TNF therapy with the number and function of M2 macrophages. The gene discussed is TNF; the disease is inflammatory bowel disease.