In addition, multiple other mechanisms could contribute to constitutive activation of the PI3K/Akt pathway in ccRCC [7], including epigenetic regulatory mechanisms, specifically microRNAs (miRNAs) [7], as well as protein complex formation with phosphoinositide-dependent kinase-1 (PDK1) and 78-kDa glucose-regulated protein [7]. This evidence concerns the gene AKT1 and nonpapillary renal cell carcinoma.