Prior studies have demonstrated that LC3-associated phagocytosis, a non-canonical form of autophagy, is an anti-inflammatory pathway during chronic liver disease and limits fibrosis progression leading us to hypothesized that albumin functions as an activator of LC3-associated phagocytosis and that its anti-inflammatory properties rely on LC3-associated phagocytosis activation. Pilot studies have demonstrated that human serum albumin enhances selective pathways of autophagy in specific blood cell sub-types from both healthy subjects and patients with cirrhosis. Validation of these preliminary observation is being performed in a larger cohort of cirrhotic patients and exploring the early signaling pathways leading to autophagy activation upon human serum albumin treatment.