For example, miR-138 leaded to cell cycle arrest by targeting cyclin D3 [37, 53], miR-138 inhibited HCC development via repressing stemness factor SOX9 expression [54], and miR-138 attenuated the adaption of cancer cells to hypoxic microenvironment by affecting the expression of HIF-1α and vascular endothelial growth factor (VEGF) [55, 56]. The gene discussed is VEGFA; the disease is cancer.