To functionally explore the role of AKT phosphorylation on mediating the effect of PI3KR3 depletion on ccRCC growth, we treated Ctrl and PIK3R3 sgRNA-infected cells with the AKT inhibitor (Capivasertib), which led to increased AKT phosphorylation but caused a decrease in AKT kinase activity (34). Here, PIK3R3 is linked to nonpapillary renal cell carcinoma.