Taken together, the abrogation of BTZ-mediated nuclear relocalization and stabilization of NRF2 by NAC aligns with the inhibition of BTZ-mediated ATF3/NOXA/cleaved caspase-3 induction and loss of cell viability by NAC and GSH-EE (Fig. 2F and 3H; Supplementary Figs. S2A and S2B, S3D–S3H), suggesting that NRF2 could be the factor connecting BTZ-induced oxidative stress to induction of ATF3/NOXA and apoptosis in Onc-p53 NSCLC cells. This evidence concerns the gene CASP3 and non-small cell lung carcinoma.