Polycystic ovary syndrome (PCOS) is a heterogeneous endocrinopathy characterized by oligo or anovulation, hyperandrogenism, and/or polycystic ovarian morphology. While women in both developed and developing nations are affected, it is also the leading cause of ovulatory infertility among women of reproductive age. This article discusses the epidemiology, risk factors, pathophysiology, diagnosis, and particular emphasis to its treatment. Global prevalence of PCOS ranges from 4 to 21% whereas it is between 9.1 and 36% among adolescents. Clinical presentation of PCOS can be mainly attributed to hyperandrogenism and chronic anovulation. Symptoms of hyperandrogenism include hirsutism, acne, and/or male pattern alopecia. Chronic anovulation proceeds with features such as oligomenorrhea, amenorrhea, and/or infertility. Even though a specific gene responsible is not found yet, it's clear that women with PCOS have two major genetic alterations involving androgen synthesis, insulin action, and also an increased incidence of other genetic alterations. Family history, obesity, and an unhealthy diet are found to be significant risk factors for the development of PCOS. The fundamental pathological changes in PCOS include hyperandrogenism, abnormality of gonadotropin secretion, and insulin resistance.  It has been noted that genes, HAS2 & CBLN1 that are associated with ovulation are expressed less in granulosa cells of PCOS patients. These cells also show significantly differentially expressed genes for transcription factors and secretory proteins in addition to having increased Toll- & NOD-like receptors. Presently, there is no universal treatment for PCOS.