The biological role of CD25 expression in AML remains unknown and the effect of IL-2 on the proliferative status of CD25+ blasts is also controversial.1 CD25 may impart environmental signals, whereas high plasma levels of enzymatically cleaved, soluble CD25 in AML may suppress the antitumor response via competition with the lymphocyte surface CD25 for IL-2 and have long been shown to be associated both with the burden and severity of the disease.14 Here, IL2RA is linked to acute myeloid leukemia.