In an effort to expand therapeutic options available to ccRCC patients in the clinical setting, we leveraged our phosphoproteomic results to prioritize the identification of phospho-substrates of kinases with current FDA-approved inhibitors, revealing signaling associated with MAPK/ERK, PI3K/AKT/mTOR, and G2/M cell cycle stalling to be elevated in ccRCC tumors and potential druggable targets. Here, AKT1 is linked to nonpapillary renal cell carcinoma.