To determine whether NRF2 is required upstream of BTZ-mediated cytotoxic signaling via ATF3/NOXA in Onc-p53 NSCLC cells, we first treated H1975 cells stably expressing NRF2 or control shRNA with vehicle or BTZ and immunoblotted cell lysates for NRF2, ATF3, NOXA, and cleaved caspase-3 (as a surrogate for apoptosis; Fig. 4D). This evidence concerns the gene CASP3 and non-small cell lung carcinoma.