Renal cell carcinoma (RCC) is a highly invasive illness with a high mortality rate, and it is the most prevalent malignant tumor of primary renal tumors. Since Protein kinase B  (AKT) is a serine/threonine kinase essential to the phosphoinositide 3-kinase (PI3K) signaling pathway, it is a promising therapeutic target for renal cell carcinoma (RCC). The reason for this research was to find out how silencing AKT affected the aggressiveness of renal cell carcinoma cells. Researchers used immunohistochemistry to quantify AKT expression in tumors and normal tissues. Caki-2 cell lines, originating from human RCCs, were used for this research. After that, RT-qPCR and western blotting were used to choose the best silencing siRNA. Researchers used a CCK8 assay, transwell assay, scratch test, and flow cytometry to examine how silencing AKT affected RCC cells. Immunohistochemical staining confirmed the presence of AKT1 expression in human renal cell carcinoma tissue. Successful silencing of AKT in Caki-2 cells. Cell growth, invasion, and migration were all slowed in studies where AKT was silenced. The progression of RCC cells from G1 to S phase could be halted and apoptosis induced in Caki-2 cells when AKT was inhibited. Immunohistochemical labeling differentiated RCC tumors from normal renal tissues regarding AKT1 expression. Together, their data suggested that members of the AKT family may play a role in the malignant progression of RCC and represent a possible therapeutic target. The results demonstrated that silencing AKT induced apoptosis in Caki-2 cells and suppressed their ability to proliferate, invade, and migrate. In addition, the progression of RCC cells from G1 to S phase was halted by silencing AKT. That’s why AKT has promise as a therapeutic target for renal cell carcinoma.