AKT1 and glioma: Pathway analysis revealed differential activation patterns across clusters in five key pathways: TP53 (cluster-specific p53 pathway alterations impacting invasion, apoptosis evasion, and stemness [26]), RTK-RAS (therapy resistance-linked transcriptional dysregulation [27]), Hippo (glioma progression and chemoresistance mechanisms [28]), TGF-β (calcium-mediated microenvironment communication [29]), and PI3K/AKT/mTOR (metabolic reprogramming associated with poor prognosis [30]).