Functional assays showed that overexpression of miR-96 in high or low glucose concentrations enhances insulin secretion and pancreatic beta-cells’ viability, whereas overexpression of PAK1 leads to cell apoptosis and impaired function of beta-cells, suggesting that miR-96 targets PAK1 and that miR-96 plays a role in the development of GDM through regulation of PAK1 and beta-cell functions and viability [168]. This evidence concerns the gene INS and gestational diabetes.