TP53 and glioblastoma: In general, strong suppression of AKT1-mTOR and a partial suppression of ERK pathways, in concert with substantial upregulation of JNK activation, the high basal or induced MAPK p38 activity, and very active p53-BAX, may promote autophagy/apoptotic commitment in glioblastoma cells, as was previously investigated [39, 41, 81, 82].