Together, our findings reveal a mechanism in which pharmacologically administered FGF1 acutely stimulates an adaptive UPR, leading to increased ER secretory capacity under pathophysiological (e.g. MASLD) conditions and a transient increase in VLDL secretion, ultimately clearing hepatic steatosis (Fig. 6H). The gene discussed is FGF1; the disease is metabolic dysfunction-associated steatotic liver disease.