AKT1 and glioblastoma: On the other hand, recent studies suggested that the gain of function of BMAL1 via adenovirus-mediated expression of BMAL1 reduced proliferation, migration, and invasion of U87MG glioblastoma cells due to the downregulation of p-AKT and Metalloproteinase-9 pathways,84 while its downregulation is associated with high proliferation rates and aggressiveness of the tumour.19