Emerging evidence implicates altered insulin receptor signaling (phosphoinositide 3-kinase/serine-threonine-specific kinase–mitogen-activated protein kinase (PI3K/AKT/MAPK) [18], androgen-mediated shifts in Wilms tumor-1 (WT1) (a transcription factor important for cell development and survival [19]), and Wingless-related integration site (Wnt)/β-catenin activity [20] in disrupting precisely coordinated hormone-induced changes in the PCOS endometrium [21,22]. The gene discussed is WT1; the disease is polycystic ovary syndrome.