This can be explained by the fact that ANGPTL-4 is a glucocorticoid-sensitive protein that is heavily upregulated in the kidney as well as peripheral tissues in the context of steroid-sensitive kidney disease, and due to being enacted through interaction with podocyte integral proteins such as podocin, which are regulated by genes such as NHPS2, mutations of these genes might be responsible for steroid-resistant nephrotic syndrome like FSGS, which might explain the significantly lower ANGPTL-4 expression in FSGS compared with its upregulation in MCD [9, 27–29]. The gene discussed is NPHS2; the disease is kidney disorder.