Given that KAT6A‐acetylated H3K23 reader TRIM24 acts as an oncogenic transcriptional coactivator[40] and high levels of H3K23ac correlated with poor prognosis of breast cancer,[41] we tested a hypothesis that KAT6A‐acetylated H3K23 recruits TRIM24–SMAD3 complex and enhances SMAD3–chromatin interaction, resulting in enhanced SMAD3 activation in breast cancer. This evidence concerns the gene TRIM24 and breast carcinoma.