In murine mammary carcinoma, tumor-derived IL-6 impaired the differentiation of myeloid progenitors, promoted the development of CD11b+Gr-1−F4/80−MHC-II− e-MDSCs, and potently suppressed T cell immunity, in which IL-6-dependent SOCS3 suppression and the consequential activation of the JAK/STAT signaling pathway are the most crucial molecular events. The gene discussed is SOAT1; the disease is neoplasm.