Exposure to EDCs can contribute to NAFLD progression by promoting the production of cytokines as well as other pro-inflammatory molecules, by inducing the polarization of KCs to a pro-inflammatory phenotype, by increasing hepatocyte proliferation and immune cell infiltration, and by favoring the transformation of HSCs to myofibroblast-like cells, thus impairing the balance between proliferation/apoptosis and, consequently, triggering liver damage and fibrosis development [359,360]. This evidence concerns the gene TBCE and metabolic dysfunction-associated steatotic liver disease.