A remedy for kidney disease successfully alters the cold shock protein response during inflammation.

Kidneys undergoing acute inflammatory responses are characterized by cell infiltration and a cytokinergic milieu. The hazard resides in the perpetuation of inflammation and ensuing fibrosis. In this issue of Kidney International, Wang et al.4 identify the cold shock Y-box binding protein-1 as the key orchestrator of cell infiltration in experimental tubulointerstitial nephritis following ureteral obstruction. Intriguingly, a small molecule previously designed to interfere with Y-box binding protein-1 interactions mediates an anti-inflammatory response and halts fibrogenesis.