Functionally, the overexpression of AHSG significantly increased the proliferation of BC cells and promoted the cell cycle from G1 to the S phase, whereas the knockdown of AHSG gave the opposite result.Additionally, western blot results revealed that AHSG expression level was negatively correlated with the phosphorylation level of Smad2/3 protein, a key downstream molecule of the traditional TGF-β signaling pathway, suggesting that AHSG could antagonize the traditional TGF-β signaling pathway. This evidence concerns the gene TGFB1 and breast cancer.