Hagemann and colleagues (2008) have reported that IL-1R/MyD88/IKKβ signal induced M2-type polarization of bone marrow derived macrophages (BMDMs), and also that transferred BMDMs from MyD88 or IL-1R deficient mice into tumor-bearing mice significantly suppressed tumor growth than those from wild type mouse. The gene discussed is MYD88; the disease is neoplasm.