In addition to the known pathways that activate hepcidin expression, we show that Ras/RAF-triggered signals and the mTOR pathway are involved in hepcidin suppression. This finding links the control of iron homeostasis with enhanced cell proliferation and anabolic growth under nutrient-rich and growth-stimulating conditions. Furthermore, we identify new components of the transcriptional machinery that control steady-state levels of hepcidin expression and hepcidin induction upon IL-6 stimulation. Among these, 3 factors (STAT6, CREBBP, and SRF) are additionally required for the BMP-triggered hepcidin response.