FOXO1 and Hyperglycemia: Furthermore, unbridled activity of FOXO1, as a result of hyperglycemia induced O-glycosylation, accounted for its disproportionate regulation of apoptotic and proapoptotic factors (decreased Bcl-2 and increased caspase-3 and BAD), thereby contributing to endothelial cell death in human aorta endothelial cells [49].