Interestingly, even in the non-mesenchymal-derived parental GBM cells such as T98G, silencing of CYBB in the TMZ-resistant clones of T98G-R still showed a potential effect of repressing NRF2 and SOD2 upregulation while downregulating mesenchymal markers to potentiate tumor suppression of TMZ treatment (Figure S2C,D). The gene discussed is SOD2; the disease is neoplasm.