In the current study, we found that the upregulation of miR-362-3p or downregulation of SP1 decreased AKT phosphorylation and significantly increased the transactivation activity of FOXO3, suggesting that miR-362-3p/SP1/AKT/FOXO3 pathway might represent a new mechanism underlying the development of RCC. This evidence concerns the gene AKT1 and renal cell adenocarcinoma.