In this study, we first investigated whether genetic inactivation of hepatocyte <i>Foxa3</i> affected the development of MASLD/MASH in C57BL/6 mice and then explored whether loss of hepatocyte <i>Foxa3</i> regulated atherosclerosis development in <i>Ldlr</i>-deficient mice. Here, LDLR is linked to metabolic dysfunction-associated steatotic liver disease.