Based upon our previous finding that a water soluble fragment of CRT covering N-terminal amino acid residues 39–272 (CRT39-272, including the N domain and partial P domain) is capable of activating myeloid cells including dendritic cells (DCs), monocytes, and macrophages though CD14/TLR4 receptor complex (14, 15), we hypothesized that tumor-derived sCRT might be able to promote MDSC generation, proliferation, and/or chemotaxis through TLR4, thereby contributing to tumor malignancy in vivo. The gene discussed is TLR4; the disease is neoplasm.