Intriguingly, inhibition of miR-140-3p expression or overexpression of KLF4, a valid target of miR-140-3p, countervailed these effects of CSF [55], which implied that CSF might relieve endothelial damage induced by DM via regulating miR-140-3p/KLF4 axis-dependent PI3K/Akt pathway. Here, AKT1 is linked to diabetes mellitus.