To further validate the role of ERK1/2 and JNK in promoting glioma apoptosis, T98G and LN18 cells were pretreated with U0126 (a MEK inhibitor) or SP600125 (a JNK inhibitor) for 2 h and then after treated with PTE for 48 h, cell proliferation and apoptosis were tested by MTT and related apoptotic proteins were assessed by western blotting.MEK is a dual-specific protein kinase that plays a role in the mitogen-activated protein kinase cascade that controls cell growth and differentiation. This evidence concerns the gene MAPK3 and glioma.