These bioinformatics and computational analyses suggest that vortioxetine suppresses glioblastoma development by modulating the functions and activities of AKT1, HIF1A, CDH1, NFKB1, and associated signaling pathways, such as the Rap1, chemical carcinogenesis-ROS, and HIF-1 signaling pathways. Here, AKT1 is linked to glioblastoma.