Moreover, an excess of SMPDL3b in human podocytes may cause the displacement of insulin receptor isoforms from caveolin-1-rich domains of the plasma membrane in a C1P-dependent manner, resulting in impaired ability to phosphorylate AKT thus promoting podocyte injury in vitro and development of DKD in vivo [6]. The gene discussed is SMPDL3B; the disease is diabetic kidney disease.