This is in line with observations in individuals with Hartnup disorder, who generally maintain amino acid homeostasis and are asymptomatic when provided with a protein-rich diet (12, 13), as well in Slc6a19-KO mice, which likewise maintain normal levels of plasma amino acids through metabolic adaptations that include limiting the use of amino acids as fuel or reducing muscle protein turnover and degradation (14, 20, 21, 27). This evidence concerns the gene SLC6A19 and Hartnup disease.