This finding supports the concept that endogenous CNP offsets the pathogenesis of MASLD/cirrhosis in the patient population and links deficits in CNP bioactivity to portal hypertension (i.e. lower levels in decompensated patients); moreover, these data dovetail well with correlations between CNP and markers of liver damage (i.e. ALT, AST). This evidence concerns the gene GPT and metabolic dysfunction-associated steatotic liver disease.