While the precise pathophysiological relevance of this elevation in the context of MASLD for these specific genotypes requires further investigation, it may suggest increased cellular stress or damage that is not directly mediated by the ApoC-III variants’ primary role in lipid metabolism, or it could be a consequence of broader metabolic perturbations linked to these genotypes, even if not directly leading to MASLD susceptibility in our cohort. This evidence concerns the gene APOC3 and metabolic dysfunction-associated steatotic liver disease.