Interestingly, patients with chronic inflammation typically develop anemia due to increased hepcidin expression in response to increased inflammatory signaling.1,8 Moreover, hypoxia-induced erythropoietin (EPO) production can suppress hepcidin expression, thereby increasing iron absorption.1,9 EPO activates the STAT5 pathway, which produces erythroferrone, which in turn suppresses the BMP/SMAD/hepcidin axis,9 a process that also involves the MAPK/ERK signaling pathway.14 The gene discussed is EPO; the disease is anemia (phenotype).