While the mechanisms by which PEAK1 regulates the expression/secretion of these factors remain to be determined, our data demonstrating that these MSC cytoprotective effects can be reversed by antagonism of activin-A in the MSC conditioned media (Fig. 7f, g) suggest that activin-A inhibition in HER2-positive breast cancers is a viable means for overcoming targeted therapy resistance. The gene discussed is ERBB2; the disease is breast cancer.