Remarkably, both PI3 K and AKT activations were partially reduced in the intensity of phosphorylation protein after luteolin treatment, whereas other key regulatory pathways, such as p38, FAK and JNK, did not affected, suggesting that luteolin could reduced PI3K/AKT activation in glioblastoma cells (Fig. 3c). The gene discussed is AKT1; the disease is glioblastoma.