This hypothesis is supported by our results in the current study showing that LGMN can activate the AKT/p65 pathway to promote GBM cell proliferation and survival, and by previous studies in epithelial ovarian carcinoma, gastric carcinoma, and breast cancer showing that LGMN stimulates tumor growth and progression via activating AKT pathways (86–88). This evidence concerns the gene AKT1 and neoplasm.