The ability of the kidney to retain plasma protein relies on a functional glomerular filtration barrier, consisting of endothelial cells, the glomerular basement membrane (GBM) and podocytes. Damage to the glomerular filter is clinically detected as proteinuria, which also is an independent predictor of the progression kidney disease (Ruggenenti et al., 2001). Within the last decades, the importance of podocytes for a functional glomerular filtration barrier has emerged. Podocytes are terminally differentiated epithelial cells with a highly organized structure, and injury to the podocyte structure appears to be a common finding in acquired proteinuric conditions (Pavenstadt et al., 2003). Identification of genes that are involved in physiological and pathophysiological functions of the podocytes is a major task. Recent studies indicate that Bestrophin (Best) 3 has cell protective functions in a number of cell types (Lee et al., 2012, Jiang et al., 2013, Song et al., 2014). In the present issue of Acta Physiologica, Golubinskaya et al. use cultured podocytes, kidneys and isolated glomeruli of the mouse kidney to provide a thorough characterisation of Best3 expression under normal conditions and in response to injury induced by endoplasmatic reticulum (ER) stress (Golubinskaya et al., 2015). Their report shed light on the complex regulation of Best3 in podocytes and will help pave the way for future studies on the pathogenesis of kidneys diseases with podocyte injury. This article is protected by copyright. All rights reserved.