This event in turn promotes KAT6A acetylation of the H3K23-mediated recruitment of the TRIM24–SMAD3 complex to chromatin, thereby increasing SMAD3 activation and the expression of immune response-associated cytokines, leading to breast cancer stem-like cell stemness, myeloid-derived suppressor cell recruitment, and enhanced metastasis in triple-negative breast cancer. This evidence concerns the gene SMAD3 and triple-negative breast carcinoma.