In patients with endometriosis, relatively larger populations of stromal and epithelial cells in the eutopic endometrium display widespread epigenetic abnormalities and mutations that favor increased estradiol and PGE2 production and action, progesterone resistance, autonomous activation of KRAS and its downstream survival pathways, and heightened cytokine production and immune cell recruitment (Figure 4). The gene discussed is KRAS; the disease is endometriosis.