Recent work supports this hypothesis, as (i) loss of PON2 in an in vitro cell model of MASLD led to disruption of pathways related to MASLD pathogenesis, including hepatic fibrosis [62], (ii) exacerbated cardiac fibrosis is reported for PON2 deficiency in a mouse transverse aortic constriction model [63] and (iii) PON2 was identified as the cellular target of vutiglabridin and necessary for alleviating MASLD-related hallmarks [64]. This evidence concerns the gene PON2 and Hepatic fibrosis.