Additionally, B7-2 expressed by AML cells has also been reported to be capable to directly provoking Th-cell responses, and subsequently, the interaction between stimulated T cells and AML cells results in upregulation of inhibitory B7-H1 and B7-DC on AML cells that may contribute to immune evasion in AML (19). The gene discussed is CD86; the disease is acute myeloid leukemia.