AKT1 and glioblastoma: In the context of GBM, HAX-1 and HSP90 interaction appears to facilitate HSP90 association with AKT1, since HAX-1 knockout leads to decreased co-localization and co-immunoprecipitation of both proteins in GBM cell lines (U118 and U87MG), and HSP90 pharmacological inhibition also impairs AKT1 phosphorylation [66].