Although moderate exposure to fatty acids increased apoB100 secretion, prolonged exposure leads to ER stress and posttranslational degradation of apoB100, and consequently decreased apoB100 secretion, both in vivo and in vitro hereby linking ER stress to NAFLD progression through apoB100 inhibition [114, 115] (Fig. 3). Here, APOB is linked to metabolic dysfunction-associated steatotic liver disease.