PTEN, which can inhibit this pathway, is lost in 50% of TGCTs [139] whereas overactivation of AKT has been observed in cisplatin-sensitive testicular tumor cells compared with their corresponding sensitive cells as a result of PDGFR-b (platelet-derived growth factor receptor beta) and PDGF-b ligand mRNA and protein levels increase [138]. The gene discussed is PDGFRB; the disease is neoplasm of testis.