The expression of sphingomyelinase-like phosphodiesterase 3b (SMPDL3b) is increased in DN podocytes, and SMPDL3b promotes degradation of ceramide-1-phosphate (C1P) to ceramides and sphingolipids, which causes the insulin receptor to shift from the caveolin-1-rich domain in a C1P-dependent manner, leading to impaired AKT phosphorylation and podocyte injury (196, 197). This evidence concerns the gene SMPDL3B and liver dysplastic nodule.