VPI increases postoperative recurrence risk by 30–50% through dual mechanisms: (1) direct dissemination via tumor penetration beyond the elastic layer, enabling pleural cavity seeding and transdiaphragmatic spread; (2) microenvironment remodeling through inflammation-driven VEGF-A overexpression (↑2.8-fold in VPI+ tumors) and lymphovascular invasion. Here, VEGFA is linked to neoplasm.