These results suggest that ER-ve cells could be more dependent on activin A for regulation of cell growth than ER + ve cells, and may utilise secretion of follistatin as a mechanism of escape from the anti-proliferative effects of activin A. There is no clear evidence to indicate why tumor cells secrete a growth inhibitor such as activin [16], suggesting it may be have alternative functions that the cells escape from by alternative mechanisms i.e. secretion of inhibitors or down regulation of receptors. Here, INHBE is linked to neoplasm.