Several mechanisms may explain this apparent contradiction: (1) PAI have additional functions beyond uPA inhibition, including activation of pathways that promote tumor growth, angiogenesis, and cell detachment [202,203,204]; (2) the PAI-1/uPA/uPAR complex can be internalized and recycled, potentially leading to increased uPAR on the cell surface and enhanced invasiveness [205]; (3) PAI-1 can elicit inflammatory responses and immune cell recruitment in the tumor microenvironment, potentially promoting a pro-tumorigenic milieu [206]. Here, SERPINB2 is linked to neoplasm.