The key genetic inactivations or mutations for RCC include those in MET proto-oncogene (MET), polybromo 1 (PBRM1), transcription factor binding to IGHM enhancer 3 (TFE3), folliculin (FLCN), Tuberous Sclerosis Complex 1 (TSC1), fumarate hydratase (FH), succinate dehydrogenase complex subunit D (SDHD), phosphatase and tensin homolog (PTEN) and VHL [10, 11], which leads to the accumulation of downstream oncogenic targets, such as HIFs [12]. This evidence concerns the gene PTEN and renal cell carcinoma.