First, increased expression scores for SH3BP2, its binding partners (PLCγ2, VAV2, etc.), and related signaling pathways in MCD and FSGS (glomerular transcriptome data) in humans was corroborated by upregulated Sh3bp2, Plcg2, and Vav2 in Sh3bp2KI/KI mice as well in in vitro studies using human podocytes. The gene discussed is PLCG2; the disease is focal segmental glomerulosclerosis.