The best biomarkers turn out to be important in pathogenesis and some become therapeutic targets—a paradigm illustrated beautifully by the herceptin receptor in breast cancer [1]. A paper in the May issue of the Journal of Clinical Investigation raises the exciting possibility that the renal biomarker, kidney injury molecule-1 (Kim-1), may become an equally important example [2]. Kim-1 (also known as Tim-1—T-cell immunoglobulin and mucin-containing molecule) was originally discovered in a screen for molecules involved in the pathogenesis of acute kidney injury (AKI)[3]. Although undetectable in normal rat kidney, Kim-1 is abundantly expressed by proliferating and dedifferentiated renal proximal tubular epithelial cells 48 h after acute ischaemic injury in kidneys examined by in situ hybridization and immunohistochemistry. The human orthologue was also identified and behaved identically. The authors concluded that ‘Kim-1 may play an important role in the restoration of the morphological integrity and function to post-ischaemic kidney’. However, subsequent data demonstrating Kim-1’s exceptional promise as a urinary biomarker for proximal tubular injury diverted much attention from its pathophysiological role. The selective expression by injured proximal tubular cells provides the foundation for Kim-1’s use as a biomarker. Furthermore, it is cleaved from the surface of activated tubular cells and released into the urine by a metalloproteinase [4]—a process regulated by the MAP kinase signalling pathways activated by cell stress [5]. This results in a close correlation between Kim-1 expression in the tissue and its excretion in urine [6], adding to its value as a biomarker. The development of sensitive immunoassays for urinary Kim-1 [6, 7] prompted an avalanche of studies over