Although this is consistent with what has been described for NRF2 activation following overexpression of the cystine/glutamate exchange system Xc-in the mesenchymal stem-like subtype of triple-negative breast cancer cells [20], because the involvement of KEAP1 cysteinylation at residues 226 and 613 in the NACET-mediated increase of NRF2 activity is demonstrated only by transient transfection experiments, we cannot exclude the possibility that other mechanisms or KEAP1 residues are involved. The gene discussed is NFE2L2; the disease is triple-negative breast carcinoma.