Preclinical studies show that alpelisib combined with other PI3K/Akt pathway inhibitors more effectively reduces Akt phosphorylation in PTEN-null GBM models than alpelisib alone, suggesting that PTEN-null GBM cells can rely on both PI3Kα and PI3Kβ isoforms to maintain cell survival [162,163]. This evidence concerns the gene PIK3CB and glioblastoma.