To explore the significance of Akt activation in the molecular mechanisms that PARK2 may contribute to tumor suppression, we tested the effect of PARK2 overexpression in PTEN wild-type (WT) (HCT116 PTEN+/+ and H1299) and PTEN mutant (PC3 and HCT116 PTEN−/−) cell line models. Here, PRKN is linked to neoplasm.