Knockout of podocyte-specific aCDase gene, Asah1, in mice resulted in an increase in total and C16 ceramide levels in glomeruli, the main substrate of aCDase, leading to foot process effacement (FPE) in podocytes, massive proteinuria and albuminuria, suggestive of nephrotic syndrome (NS) [44]. This evidence concerns the gene ASAH1 and Netherton syndrome.