An unexpected role of steroid on podocytes: from zebrafish to human nephrotic syndrome?

In this issue of Kidney International, Jobst-Schwan et al. developed a zebrafish model of MAGI2-deficiency, which recapitulates findings of human nephrotic syndrome due to MAGI2 mutations. The authors use this model system to screen for drugs that might target and alleviate MAGI2-associated nephrotic syndrome pathways. The scientific context of this publication and the significance of its key findings are discussed in this commentary.