A 6-month-old male infant presents with lethargy, poor feeding, and vomiting. Serum ammonia is markedly elevated at 180 µmol/L (normal <50). Plasma amino acid analysis shows elevated glutamine and alanine. Genetic testing reveals a homozygous loss-of-function mutation in NAG synthase. The structure marked **A** in the urea cycle diagram is the rate-limiting enzyme of ammonia detoxification. Which of the following best explains why NAG synthase deficiency presents clinically identical to CPS-1 deficiency despite normal CPS-1 protein expression?