Diabetic nephropathy (DN) is worldwide the leading cause of end-stage renal disease (ESRD), which requires dialysis or a kidney transplant. Diabetes impacts negatively on all cells of the kidney. Podocyte cell injury has been shown to be a major driver in the initiation and progression of DN. The podocyte actin cytoskeleton plays an essential role in the proper organization and function of the glomerular filtration barrier. In this study, we describe a new interaction partner of podocyte actin organization, coronin, actin binding protein, 2B (CORO2B). CORO2B has already been associated to the connection of the plasma membrane with the actin cytoskeleton in neuronal cells. In human DN patients, CORO2B is downregulated. In fish, there are two coro2b genes, coro2ba and coro2bb. We initially employed a morpholino-based approach to elucidate the role of the coro2b genes in the zebrafish pronephros. The morphant larvae showed abnormal morphology of the pronephros, with fewer podocytes, as well as hydrocephalus. At a functional level, proteinuria was observed in collected fish water suggesting a functional defect in the glomerular filtration barrier. Mammalian podocyte cell culture experiments show that CORO2B is crucial for the organization and maintenance of the actin skeleton of podocytes and by extension, the glomerular filtration barrier. These data are currently being validated by a CRIPSR knockout strategy in zebrafish.