It may indicate the potential presence of an interaction between VEGFR3 and Plexin A1 in PBMCs as co-receptors to enhance the binding of pro-tumorigenic ligands and stimulate VEGFR3 activity or tumor immune evasion and thus, negate the tumor suppressive nature of Plexin A1 signaling. The gene discussed is FLT4; the disease is neoplasm.