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]. Here, ASAH1 is linked to nephrotic syndrome.