The metabolic error in I-cell disease (i., deciency of phosphotransferase activity) gives rise to a secondary phenotype of generalized diminished…

The metabolic error in I-cell disease (i.e., deficiency of phosphotransferase activity) gives rise to a secondary phenotype of generalized diminished lysosomal enzyme activity. What other metabolic defects in the mannose 6-phosphate-mediated uptake system could result in such a phenotype, and how could you confirm the defect?