The upregulation of CFTR observed in PCOS model and induced by DHT in α cells, together with the suppressed blood glucagon/glucose levels in PCOS model and DHT-suppressed glucagon release by α cells, which can be reversed by CFTR inhibitors, suggest that the impaired glucagon levels observed in PCOS patients are likely to be due to the hyperandrogenism-induced upregulation of CFTR, since hyperandrogenism is a hallmark of PCOS (Gambineri et al., 2002; Azziz et al., 2006). This evidence concerns the gene GCG and polycystic ovary syndrome.