We confirm that C-PC selectively targets GBM cells by enhancing cellular uptake in resistant phenotypes while sparing normal cells, and that C-PC-CDDP combination therapy enhances cytotoxicity significantly in treatment-sensitive U87 cells through apoptosis induction and ROS modulation, the latter involving upregulated MnSOD and catalase expression, and C-PC monotherapy offers superior efficacy compared to combination treatment in CDDP-resistant U87-EGFRvIII cells. This evidence concerns the gene SOD2 and glioblastoma.