Using a combination of in vivo, ex-vivo, and in vitro models, we show that macrophages play a key role in endometriosis-associated hyperalgesia, that disease-modified macrophages exhibit increased expression of IGF-1, and that inhibition of macrophage-derived IGF-1 can attenuate nerve growth and expression of nociceptive genes in vitro. The gene discussed is IGF1; the disease is endometriosis.