As mentioned above, STAT3 and Akt/PKB are known to be consistently upregulated in various glioblastoma cell lines due to leptin/ObR overexpression, which drives dysregulation of the cell cycle suppressor Rb (retinoblastoma protein), thus promoting uncontrolled cellular proliferation in the absence of normal suppressive mechanisms (Figure 1) [23]. Here, AKT1 is linked to glioblastoma.