Reported downregulation of Phosphatase and Tensin Homolog (PTEN) in investigated glioma cell lines [68,69,70], upregulation of AKT signaling and high level of activity of GSK3, might provide the mechanistic ground for gp120-driven proliferation and metabolic switch specifically in gliomas but not in other investigated cancer cell lines. The gene discussed is AKT1; the disease is central nervous system cancer.