Additionally, VEGFR3 and VEGFR2 form heterodimers in both BECs and LECs upon VEGF-A or VEGF-C stimulation (Dixelius et al., 2003; Nilsson et al., 2010), and previous studies have underlined the contribution of VEGFR2/VEGFR3 heterodimers to VEGF-C-driven tumor and corneal lymphangiogenesis and pulmonary lymphangiectasia (Yao et al., 2014; Durre et al., 2018). This evidence concerns the gene KDR and neoplasm.