For example, reduced FOXO1A expression may contribute to the pathogenesis of glioblastoma through deregulation of TGFβ cytostatic signalling in neuroepithelial cells [9] while aberrant stoichiometry of FOXO1A-androgen receptor interactions may promote AKT-dependent and -independent survival of prostate cancer cells [13,16]. Here, FOXO1 is linked to glioblastoma.