In addition, we also recently showed that the same treatment improved the laboratory data of 2 mitochondrial disease patients, one with mitochondrial cardiomyopathy and the other with mitochondrial diabetes, and brain natriuretic peptide (BNP) decreased by 31% in the former patient, and in the latter, insulinogenic index increased by 3.1 fold.[63] Taken together, these data suggest that our treatment may improve disorders induced by cellular ATP shortage, which can be considered a reason for the abnormalities found in mitochondrial disease patients.[64]. The gene discussed is NPPB; the disease is inborn mitochondrial metabolism disorder.