We next generated GBM cell lines stably overexpressing wild-type Src (SrcWT) or the catalytically inactive mutant SrcK295M (hereafter named Src kinase-dead, SrcKD) in which we could once again recapitulate that Src activity is significantly inhibited after SrcKD overexpression (Fig 2G and H) and required to sustain NRF2 (Fig 2G, I, and J). Here, SRC is linked to glioblastoma.