Polycystic ovary syndrome (PCOS), which causes problems such as anovulation, hyperandrogenism, and infertility, is the most common endocrinopathy of the reproductive period and is associated with an increased risk of several disorders such as dyslipidemia, cardiovascular disease, insulin resistance, and type 2 diabetes. 1,2 Today, there are different diagnostic criteria for PCOS determined by different consensuses. [2][3][4][5] Hyperandrogenism was included in all of these diagnostic criteria, except for PCOS patients with phenotype D, which is within the Rotterdam criteria and accompanied by oligoanovulation and polycystic ovaries. 2 In addition to hyperandrogenism, luteinizing hormone (LH) hypersecretion and increased LH/ follicle-stimulating hormone ratio have also been demonstrated in patients with PCOS. 6,7 Increased LH secretion is seen as one of the causes of hyperandrogenism in PCOS and hyperandrogenism is one of the most important factors that is involved in the pathogenesis of this syndrome. 7 Hyperandrogenism is seen in approximately 60% of patients with PCOS and is one of the responsible factors for symptoms and findings such as anovulation, subfertility, acne, and hirsutism in these patients. 4,5 Although androgens contribute to follicle maturation and development at physiologic levels, they arrest folliculogenesis in the case of hyperandrogenism, as in PCOS. 8,9 The human oocyte is arrested in the diplotene stage of meiosis 1 until the meiotic resumption is triggered by LH. To date, it has been demonstrated that there are many factors in the provision of the meiotic arrest. In recent years, some evidence has been reported regarding the relationship of C-type natriuretic peptide (CNP) with this process. CNP belongs to the natriuretic peptide family and is encoded by the natriuretic peptide precursor C. In the ovary, it is mainly secreted from follicular granulosa cells to follicular fluid and acts through the natriuretic peptide receptor 2 (NPR2). 10,11 The binding of CNP to NPR2, a guanylyl cyclase, increases the release of cyclic guanosine monophosphate (cGMP), leading to meiotic