To confirm these results, they experimented on NHPS2-ANGPTL4 transgenic rats and extrapolated that the ANGPTL-4, via complex interplay with the podocyte-GBM interface, results in foot process effacement, and that mutation of the NHPS2 gene, which encodes the podocyte protein podocin, results in a steroid-resistant variant of nephrotic syndrome, namely FSGS [9]. Here, ANGPTL4 is linked to nephrotic syndrome.