However, BEVs are heterogeneous, and BEVs produced from different strain sources as well as different survival environments are usually very different; for example, H. pylori-derived BEVs induce hepatic fibrosis progression in liver fibrosis through activation of HSCs as well as modulation of autophagy, but in hepatocellular carcinoma, H. pylori-derived BEVs promote tumor progression through activation of the TGF-β signaling pathway (Zahmatkesh et al., 2022; Shegefti et al., 2023; Mohammadi Azad et al., 2024). Here, TGFB1 is linked to neoplasm.