AKT1 and glioblastoma: AEBP1, another gene in the signature, plays a role in organizing and remodeling ECM and acts as a transcriptional repressor.[52,53] AEBP1 overexpression can activate the NF-κB and PI3K-AKT pathways, thereby promoting tumor development in many malignancies, such as breast cancer, glioblastoma, and bladder cancer.[52] Additionally, Robert et al[54] demonstrated that ASPN, a novel factor of mesenchymal stromal cells and fibroblasts, could regulate the TME and promote metastatic progression.