Endometriosis has been traditionally viewed as a hormone-dependent disease where gonadic estrogens stimulate the proliferation of endometriosis implants, enhance chronic inflammation and prompt painful symptoms. Recently a more comprehensive understanding of this disease profiles endometriosis as an abnormal hormonal microenvironment characterized by increased estrogen responsiveness, progesterone resistance and aberrant estrogens synthesis and metabolism. This latter feature, other way defined intracrinology, plays a crucial role in sustaining the loop between estrogens, inflammation and pain. Further profiling intracrinology in endometriosis offers new basis for phenotypic characterization of the disease, drives the understanding of potential mechanisms of drug resistance and identifies new therapeutic targets.