Thus, because this IL17-A release occurred in response to T cell specific stimulation (anti-CD3 + anti-CD28) the most likely explanation for the increased levels is that the ability of circulating T cells to release IL17-A is maintained in the presence of primary AML cells even though these cells show constitutive release of several immunoregulatory cytokines [21]. The gene discussed is IL17A; the disease is acute myeloid leukemia.