PLCG2 and nephrotic syndrome: The following outlines the results demonstrating upregulation of SH3BP2, its binding partners, and signaling pathways in individuals with nephrotic syndrome, followed by results using Sh3bp2KI/KI mice with a gain-in-function mutation demonstrating a phenotype of nephrotic syndrome, and verifying the expression of SH3BP2, PLCγ2, and VAV2 in human and mouse podocytes.