Thus we stress that our findings of altered amino acid serum levels might imply subtle rather than frank heart failure42,43, a hypothesis supported by the fact that we found no correlation of any of the metabolites with the traditional marker for heart failure, NT-proBNP, nor with the traditional marker for inflammation C-reactive protein, and by the fact that neither by traditional clinical-laboratory means nor by metabolomic (Fischer ratio) criteria did we find any evidence for important (Fontan-associated) liver disease in our patients. The gene discussed is NPPB; the disease is liver disorder.