We determined the phenotype of this expanded Treg population and confirmed that BE from NAFLD-HCC subjects induced the expansion of effector IL-10+ Tregs (CD3+CD4+CD25+Foxp3+IL-10+) compared to non-NAFLD control BE (P = 0.011) (Supplementary Fig. 5a). Here, FOXP3 is linked to metabolic dysfunction-associated steatotic liver disease.