SLC22A17 and bacterial infectious disease: This potential mode of action has been supported by the identification of a cellular receptor for NGAL (NGAL-R/hLCN2-R in humans or 24p3-R/mLCN2-R/rLCN2-R in mouse and rat, also called SLC22A17), which promotes the endocytosis of both free and iron-bound NGAL, together with the discovery of small molecules that may act as mammalian siderophores and can preserve the iron binding properties of NGAL in the absence of bacterial infection (14, 15).