C1QBP and neoplasm: Moreover, the depletion of MIF led to a significant reduction in PMNs, suggesting a pivotal role of exosome-derived MIFs in promoting a fibrotic and immunosuppressive microenvironment in hepatic PMNs. Further analysis suggested that treatment of HSCs with tumor-derived exosomes promoted membrane transport of complement C1q binding protein (C1QBP) and CD44v6 complex, mediated by insulin growth factor-1.