Consequently, while all models confirmed the pro-metastatic role of MASLD, the observed effects in MCD/CDAHFD models primarily reflect the impact of the hepatic microenvironment (e.g., MIF secretion and stromal remodeling), whereas the HFHCD model, encompassing the systemic metabolic dysregulation characteristic of human MASLD, including obesity, insulin resistance, and adipose tissue inflammation, suggests that these broader metabolic alterations may independently influence tumor progression and metastatic behavior through endocrine signaling or systemic immune modulation. This evidence concerns the gene MIF and neoplasm.