During the pathogenesis of these malignancies, the over-expression of Axna2 acted as a co-receptor of plasminogen and the tissue plasminogen activator, which could convert plasminogen to plasmin and contribute to increase plasmin activity on the tumor cell surface, mediate extracellular matrix degradation and promote neoangiogenesis, resulting in the promotion of tumor growth [29–31]. Here, PLG is linked to neoplasm.