One of the main drivers of HSCs activation, suggests that E. coli-derived BEVs may promote HSCs activation by activating the TGF-β signaling pathway, and further animal experiments revealed that when E. coli-derived BEVs were translocated to the liver, the expression of the liver fibrosis markers, α-SMA and Collagen I, was found to be significantly elevated by immunohistochemical staining (Dorner et al., 2024). The gene discussed is TGFB1; the disease is Hepatic fibrosis.