Concurrently, the aberrantly activated PI3K/Akt pathway not only promotes B-cell survival, antibody class switching, and the formation of immune complexes—all of which contribute to renal injury—but also stimulates the proliferation of glomerular mesangial cells and the deposition of extracellular matrix, thereby accelerating glomerulosclerosis. The gene discussed is AKT1; the disease is glomerulosclerosis.