Previously, it has been demonstrated that in MCF7 breast cancer cells, STAT3 collaborates with FRA1 and c-JUN AP1 components to activate the MMP9 promoter [28], while in HepG2 hepatoma cells, STAT3 associates with HDAC1 to inhibit IL6-induced CCL2 transcription [29]. This evidence concerns the gene CCL2 and breast carcinoma.