In addition, we aimed to explore other critical downstream targets and their possible underlying signaling mechanisms contributing to the progression of ccRCC such as phosphoinositide 3-kinase (PI3K)/AKT/mTOR, autophagy, and Wnt/β-catenin pathways, and assess any possible differential activation of these signaling hubs between Caki-1 and Caki-2 cells. This evidence concerns the gene AKT1 and nonpapillary renal cell carcinoma.