We also demonstrated that overexpression of SMPDL3b in podocytes can lead to impaired phosphorylation of AKT in a C1P-dependent manner, thereby promoting podocyte injury in DKD, while podocyte-specific deletion of SMPDL3b or exogenous C1P administration rescues podocyte loss and prevents proteinuria [29]. This evidence concerns the gene AKT1 and diabetic kidney disease.