Our observations of immune status in the untreated AML patients were consistent with increased lymphocyte exhaustion, as previously reported [13,14,15], including enhanced PD-1 immune checkpoint expression [34], decreased DNAM-1 activating receptor expression on NK cells [35], and potent upregulation of the exhaustion and immunosuppressive marker CD39 on B, NK, and CD4+ T lymphocytes. The gene discussed is CD226; the disease is acute myeloid leukemia.