The stabilized PTEN inhibited the proliferation of ccRCC cells by suppressing the phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT) and tumor necrosis factor-α/nuclear factor kappa-B (TNF-α/NF-kB) signaling pathways, and at the same time, enhanced the sensitivity of cancer cells to tyrosine kinase inhibitors (TKIs) [23]. This evidence concerns the gene AKT1 and nonpapillary renal cell carcinoma.