Moreover, secondary galactosemia due to citrin deficiency might be involved in the NICCD pathogenesis—the increased cytosolic NADH/NAD+ ratio in citrin-deficient hepatocytes might inhibit the activity of uridine diphosphate- (UDP-) galactose-4-epimerase [33], leading to accumulation of a large quantity of galactitol and galactonate [34], and galactitol has been suggested as one of the substrates causing jaundice, hepatosplenomegaly, hepatocellular insufficiency, and cataracts [30, 35, 36]. This evidence concerns the gene SLC25A13 and hyperinsulinemic hypoglycemia, familial, 4.