In juvenile neuronal ceroid lipofuscinosis, which is caused by mutations in the CLN3 gene, neuronal GalCer expression and transport is important and thus a defect in the anterograde transport of GalCer from the trans-Golgi to lipid rafts of plasma membrane affects the proper composition, structure, and function of plasma membranes, which, in turn, leads to deregulation of ceramide levels with an end effect of increased neuronal apoptosis [57]. This evidence concerns the gene CLN3 and neuronal ceroid lipofuscinosis.