In contrast, all tested brain tumor cell models were sensitive to a triplet therapy, in which AKT and PDK inhibition was combined with the pharmacological reactivation of protein phosphatase 2A (PP2A) by NZ‐8‐061 (also known as DT‐061), DBK‐1154, and DBK‐1160. This evidence concerns the gene AKT1 and brain neoplasm.