We discovered that knockdown of matriptase-2 (mtp2), a protease which cleaves membrane-bound hjv[17], produced anemia, accumulation of intraembryonic iron, and increased hepcidin expression in zebrafish embryos, however, surprisingly, mtp2′s effect on hepcidin expression was independent of hjv. Thus the zebrafish embryonic model of hepcidin regulation (Figure S12) differs from the mammalian model, which was derived from in vitro studies, human patients, and post-natal animal models. The gene discussed is HJV; the disease is anemia (phenotype).