Also, an in vitro study on human cavernous endothelial cells (hCECs) exposed to a diabetic-like environment, showed that overexpression of miR-126-3p ameliorates endothelial dysfunction by regulating the mitogen-activated protein kinase (MAPK) signaling pathway, by reducing the expression of its target gene, Sprouty-related protein with an EVH1 domain (SPRED1)36. The gene discussed is WNK2; the disease is endothelial dysfunction.