Parallel expression/secretion of Lcn2-R and Lcn2 under conditions of renal medullary hyperosmolarity, which may be encountered during early stages of bacterial infection, would be deleterious for two reasons: 1) autocrine or paracrine endocytosis of secreted (apo-)Lcn2 would promote cell damage [8] (see also Figs. 3 and 6) rather than limit the insult; and 2) endocytosis of Lcn2 via Lcn2-R would reduce the availability of Lcn2 in the lumen and thereby reduce the siderophore-Fe3+ scavenging and bacteriostatic effect of apo-Lcn2. The gene discussed is LCN2; the disease is bacterial infectious disease.