Notably, the MASLD/MASH-prone WD-fed C57BL/6J mouse strain exhibited impaired de novo NAD+ synthesis pathway, marked by reduced protein levels of tryptophan-2,3-dioxygenase and kynurenine 3-monooxygenase, pivotal for initial tryptophan degradation, and elevated levels of proteins downstream of ACMSD, while maintaining stable ACMSD protein levels (Fig. 4C). This evidence concerns the gene KMO and Wilson disease.