In human glioma cells without PTEN, reintroducing wild-type PTEN, inhibiting PI3-kinase using LY294002, or blocking AP-1 activity with dominant-negative Jun and Fos all led to reductions in PDPN expression, indicating that the heightened expression of PDPN in human glioblastoma is linked to the loss of PTEN function and activation of PI3K-AKT-AP-1 signaling [92]. The gene discussed is PTEN; the disease is central nervous system cancer.