Recently discovered peptide hormone hepcidin is the key regulator of systemic iron homeostasis. Iron metabolism is regulated in response to variations in hepcidin plasma levels. Hepcidin levels that are inappropriately low or high result in iron overload or iron deficiency, respectively. The early studies showed that hypoxia, iron concentration, and inflammation influence hepcidin levels, but the exact mechanism remained elusive. Very recently, different research groups discovered that IL-6, through the Jak/STAT-3 signaling pathway, is involved in regulation of hepcidin levels in response to inflammatory stimuli. In this review we present a general view of hepcidin biology, with emphasis on regulation in inflammatory conditions.