To assess whether increased phosphorylation, and thus kinase activity, of MAPKAPK2 is causally related to decreased viability upon oxidative stress in our GBM cell models, we next pretreated U87MG and U251MG cells with 10 μM PF-364402 (MAPKAPK2 inhibitor, MK2i) before exposing them to t-BHP (Fig. 4E). The gene discussed is MAPKAPK2; the disease is glioblastoma.