The PI3K/Akt/mTOR and MAPK/ERK pathways are central to GBM progression, with PI3K/Akt/mTOR hyperactivation often due to PTEN loss or receptor amplification driving growth, metabolism, survival, and chemoresistance, whereas MAPK/ERK signaling promotes mitogenic transcription and cell cycle progression (Shahcheraghi et al. 2020; Khabibov et al. 2022). The gene discussed is AKT1; the disease is glioblastoma.