Additionally, synergistic treatment with naringin (243 μM) and temozolomide (212.5 μM) induced apoptosis in glioblastoma cells by increasing p53 and caspase-3 levels and decreasing Bcl-2 levels through inhibition of the PI3K/Akt pathway and DNA repair mechanisms (PARP-1 and MGMT) (Figure 4) [131]. Here, AKT1 is linked to glioblastoma.