Unlike enzyme deficiencies found in traditional lysosomal storage diseases (LSDs), however, NPC1 protein does not secrete itself from cells, making cross-correction unlikely through transduced cells alone; therefore, to achieve clinical benefits over CNS storage diseases with enzyme deficiencies alone, technical challenges would need to be met in order to achieve clinical benefits in comparison to CNS storage diseases caused by enzyme deficiencies alone [149]. This evidence concerns the gene NPC1 and hyperinsulinemic hypoglycemia, familial, 4.