AKT1 and glioblastoma: For example, NSAIDs have been shown to inhibit the Akt/mTOR pathway, which is frequently dysregulated in GBM and plays a role in cell survival, proliferation, and angiogenesis.[52] NSAIDs have also been shown to modulate the Wnt/β-catenin pathway, which is involved in GBM stem cell self-renewal and differentiation.[53] These findings suggest that NSAIDs may have pleiotropic effects on multiple pathways involved in GBM development and progression.