Further mechanistic insights from the group of Mukhtar revealed that the overexpression of HO-1 driven by constitutive NRF2 activation was able to increase the resistance of A549 NSCLC cells to the proxidant EGCG, a phenotype reverted by HO-1 silencing, as well as the inhibition of NRF2 nuclear translocation and iron chelation by Desferoxamine (DFO) [136]. The gene discussed is HMOX1; the disease is non-small cell lung carcinoma.