Moreover, when vorinostat is used as a combined therapy with gefitinib or erlotinib, which are EGFR-TKIs, it can promote oxidative stress-dependent apoptosis by the suppression of the c-MYC-regulated NRF2 functions and increase the levels of KEAP1 in NSCLC cells [94]. The gene discussed is NFE2L2; the disease is non-small cell lung carcinoma.