We showed that 1) breast cancer cells promote the expansion, chemotactic migration, and immunosuppressive function of Tregs and that 2) ZA inhibits the ability of breast cancer cells in a dose-dependent manner to promote Tregs proliferation, migration, and function at least partially due to the ZA-induced reduction of breast cancer cell expression of selected factors/chemokines (CCL2, CCL5, IDO, etc.). This evidence concerns the gene CCL2 and breast carcinoma.