Taken together, our data support a potential dual mechanism of action of ZOL on the activin signaling pathway in ER-ve breast cancer cells in vitro and in vivo; firstly via a decrease in follistatin secretion leading to an increase in the tumour suppressor pSmad2C, and secondly via a decrease in nuclear localization of the tumour promotor pSmad2L. The gene discussed is FST; the disease is neoplasm.