Similarly, podocyte-specific deletion of Asah1 was shown to induce podocytopathy and nephrotic syndrome in mice due to ceramide-induced oxidative stress followed by apoptosis in glomeruli [76] and lysosomal dysfunction [77], while lysosomal deficiency of Asah1 led to the development of membranous nephropathy, FSGS and minimal change disease [74]. The gene discussed is ASAH1; the disease is nephrotic syndrome.