Myeloid cells derived from bone marrow contribute to the formation of the premetastatic microenvironment[42] and persistent production of immune response‐related cytokines in tumor cells increases MDSCs recruitment, resulting in the promotion of CSC properties, cancer immune escape, and metastasis.[7, 24, 43] Thus, we investigate whether upregulation of IL‐6, IL‐22, and TNFα by the KAT6A–SMAD3 axis described above is critical for breast cancer stem‐like cell (BCSC) properties in TNBC. The gene discussed is KAT6A; the disease is neoplasm.