Together with the findings that CFTR modulates p-CREB expression and downstream targets in ovarian granulosa cells in both CF and PCOS (Chen et al., 2012), we hypothesized that CFTR may be involved in the regulation of glucagon production by modulating p-CREB in α cells, and that defect or expression alteration of CFTR may dysregulate the glucagon levels, contributing to abnormal glucose levels as seen in CF and PCOS. This evidence concerns the gene CREB1 and polycystic ovary syndrome.