Results from preclinical studies suggest that enzyme replacement strategies represent promising treatment options for NCLs caused by the dysfunction of soluble lysosomal enzymes, such as palmitoyl-protein thioesterase 1 (PPT1) in CLN1 disease, tripeptidyl peptidase 1 (TPP1) in CLN2 disease or CTSD in CLN10 disease [8,99,100,101,102]. This evidence concerns the gene PPT1 and neuronal ceroid lipofuscinosis 10.