Specifically, Fbxo22 is deleted in various organs in combination with other established genetically modified mouse tumor models such as tumor suppressor inactivation (Ptenfl/fl, p53fl/fl, or Lkb1fl/fl), particularly PTEN, p53, and LKB1 acting as the substrates of FBXO22, or oncogene activation (e.g. KRasG12D). This evidence concerns the gene PTEN and neoplasm.