For example, chronic myeloid leukemia cells that are resistant to imatinib therapy show more expression of nuclear HO-1, and drug resistance could be reversed by the addition of E64d, a protease inhibitor, or the combination siRNA to imatinib treatable, to impede HO-1 nuclear migration, thus enhancing imatinib-induced cytotoxicity (Tibullo et al., 2013). The gene discussed is HMOX1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.