Although every single VEGF paralog in humans (PlGF, VEGF-B, VEGF-C, VEGF-D) has been proposed to mediate the tumor escape under anti-VEGF-A treatment (Li et al., 2014; Lieu et al., 2013), only VEGF-C and VEGF-D activate VEGFR-2 and VEGFR-3 (Achen et al., 1998; Joukov et al., 1996) and are therefore prime suspects (Kubota, 2012; Li et al., 2014; Stacker et al., 2001; Wang and Tsai, 2015). This evidence concerns the gene KDR and neoplasm.