Conversely, treatment of monocyte-derived DCs with FST has previously been shown to rapidly increase CXCL10 secretion, indicating direct inhibition also by autocrine Activin signaling.23 TAMs expressing CSF1R are not essential to mediate T cell exclusion by Activin-A, since their depletion did not slow INHBA-dependent tumor growth. The gene discussed is FST; the disease is neoplasm.