In this study, we constructed IL-6-knockdown 4T1 murine mammary carcinoma-bearing models to study the effects of tumor-derived IL-6 on the development of e-MDSCs in vivo to determine whether SOCS3 deficiency and sustained activation of the JAK/STAT signaling pathway blocked the differentiation of myeloid linkage and promoted the recruitment of e-MDSCs locally. The gene discussed is SOAT1; the disease is breast carcinoma.