Additionally, VEGFR2 interacts with c-Met (hepatocyte growth factor receptor) in a heterocomplex (Fig. 5b), where VEGF-A recruits protein tyrosine phosphatase 1B (PTP1B) to dephosphorylate c-Met, inhibiting its signaling and reducing tumor cell migration and invasiveness.147 VEGFR3 also forms a complex with NRP2 (Fig. 5c), enhancing lymphangiogenesis and supporting EC survival.148 VEGF-C stimulation strengthens this interaction, leading to increased VEGFR3 phosphorylation and activation of downstream signaling. This evidence concerns the gene FLT4 and neoplasm.