In breast cancer, tumor-derived IL-6 predominantly modulates the differentiation and immunosuppressive ability of MDSCs at both the tissue and cellular levels in which the soluble CD126-mediated IL-6 trans-signaling pathway and SOCS3 suppression are the most crucial molecular events orchestrating IL-6-dependent sustained activation of the JAK/STAT pathway in breast cancer MDSCs. This evidence concerns the gene SOAT1 and neoplasm.