SOD1 and glioblastoma: In the same way, negative regulation of SOD-1, as well as the addition of TNF-α to GBM cells, generate increase in the ROS production, leading to SOD-1 decline in a exposure time-dependent manner, and to rise the phosphorylation of AKT in a redox status-dependent manner, which induces the reorganization of the actin cytoskeleton (52).