Surprisingly, a large body of evidence also indicates a contributing role of ERK1/2 activation in cancer cell apoptosis primarily induced by chemical compounds, including glioblastoma, bladder, breast, colon, endometrial, head and neck, lung, renal cell, and testicular germ cell carcinomas [76,77,78,79,80,81,82,83,84,85], and mechanically, through activation of caspase 3 and induction of reactive oxygen species. Here, CASP3 is linked to glioblastoma.