In the eight experimental groups, SERPINA1 knockdown reversed ITGB3 overexpression-induced effects, normalizing PCNA/Vimentin elevation and E-cadherin suppression (P < 0.05)(Fig. 4e-h), establishing ITGB3 as the primary effector of SERPINA1-mediated tumor progression. The gene discussed is ITGB3; the disease is neoplasm.