AKT1 and glioblastoma: In addition, the SCP2-specific inhibitor itraconazole slowed the trafficking of cholesterol from late endosomes and lysosomes to the plasma membrane by reducing the level of SCP2, resulting in repression of the AKT1-mTOR signaling pathway, induction of autophagy, and, ultimately, inhibition of cell proliferation in glioblastoma [19].