Moreover, in NOD/SCID mice, silencing of Nur77 and Nor1 reduced the antiAML activity of Z-LIG, suggesting Z-LIG has the potential to function as a new bifunctional agent in the treatment of AML, as it has the ability to restore both apoptosis and differentiation mediated by Nur77/Nor1 [77]. The gene discussed is NR4A1; the disease is acute myeloid leukemia.