AR and Insulin resistance: Because the endometrial epithelial cells and decidual and non-decidual stromal cells are the major cell types that express AR [24, 51, 52, 74], we hypothesized that the uterine epithelial and stromal/decidual cells modulate immune cell-mediated inflammatory responses through paracrine-regulated AR signaling pathways that are activated under conditions of hyperandrogenism and insulin resistance.