In our GBM models, we found that in response to oxidative stress PME-1 overexpression, by inhibiting nuclear PP2A-B55α activity, increased the phosphorylation (and activation) of MAPKAPK2 Thr334, to promote subsequent RIPK1 Ser320 phosphorylation, and finally, cell death. The gene discussed is PPME1; the disease is glioblastoma.