Importantly, NT1721 also induced apoptosis in CD34+/CD38−/CD96+ KG1a leukemic stem-like cells that displayed resistance to clinically used AML drugs, i.e. cytarabine and sorafenib, suggesting that NT1721 may be a valuable new agent for the treatment of drug-resistant AML. The gene discussed is CD96; the disease is acute myeloid leukemia.