These data support previous reports showing that aberrant TLR signaling in early hematopoietic progenitors is associated with a high risk of AML transformation (32) and that increased expression of TLR2 and signaling intermediates (like MyD88) is also seen in the bone marrow of patients with AML with no response to induction therapies compared with those that experience complete remission (32). The gene discussed is TLR2; the disease is acute myeloid leukemia.