SMAD3 was identified as a non-histone substrate of lysine acetyltransferase 6 A (KAT6A) and the acetylation of SMAD3 at K20 and K117 by KAT6A leads to enhanced breast cancer stem-like cell stemness, myeloid-derived suppressor cell recruitment, and triple-negative breast cancer (TNBC) metastasis [21]. This evidence concerns the gene SMAD3 and breast carcinoma.