The inducible mouse model of podocyte inactivation of NPHS2 was presented earlier to develop NS with albuminuria, hypercholesteremia and hypertension with progressive podocin loss and at 4 weeks after induction of NPHS2 deletion, an FSGS is fully established.3 Thus, the aim of the study was to characterize this inducible mouse model of podocyte inactivation of NPHS2 with respect to volume handling and proteinuria, to carefully examine the timeline of the symptom appearance and to identify new mechanism for the dysregulated sodium handling during the development of NS. This evidence concerns the gene NPHS2 and Netherton syndrome.