Interestingly, it has also been reported that NAFLD reduces the activity of DDAH in humans (the Framingham Heart Study Third Generation Cohort), leading to reduced concentrations of circulating CIT and increased concentrations of circulating ADMA; therefore, there is more available ADMA for conversion into DMGV by the enzyme AGXT2 [40]. This evidence concerns the gene DDAH1 and metabolic dysfunction-associated steatotic liver disease.