We therefore may propose a model involving two different internalization routes for either ATF-SAP chimera or pro-uPA-SAP conjugate: an LRP1 and ligand-independent endocytosis, induced by the ATF binding to uPAR, mainly detected on LRP1 negative cancer cells, but not on MDA-MB-231; an LRP1 and ligand-dependent endocytosis, responsible for the pro-uPA-SAP endocytosis observed in LRP1 positive fibroblasts (Fig. 8). The gene discussed is PLAUR; the disease is cancer.