In other words, the mouse model used in this study recapitulates several important features of human adenomyosis, i.e., inflammation and angiogenesis as displayed by the constitutive activation of NF-κB and increased COX-2 but decreased PR-B expression in adenomyotic lesions, increased uterine weight and presumably enlarged uterus, increased generalized hyperalgesia, and elevated uterine contractility, due possibly to elevated myometrial OTR expression. The gene discussed is NFKB1; the disease is adenomyosis.