VHL and neoplasm: Numerous mouse models have supported this notion of genetic cooperation by showing that renal epithelial cell-specific inactivation of different combinations of Vhl together with Pten10, Tsc111, Pbrm111–13, Bap111,14, Trp5315, Trp53/Rb116, Cdkn2a17, or with Myc17 overexpression causes the formation of cystic and solid precursor lesions or ccRCC tumours.