Experimental HSP90 inhibitors like 17-AAG [177] as well as nelfinavir and ritonavir inhibit AKT function [161, 185-190], partially reversing faulty PTEN function as commonly seen in, and forming one of the core growth enhancing abnormalities of, glioblastoma [191-193]. The gene discussed is AKT1; the disease is glioblastoma.