Furthermore, CRIVi45–51 demonstrated a greater potency in inhibiting EC proliferation than other antiangiogenic proteins (endostatin and angiostatin) and peptides (anginex and cilengitide) already tested in cancer clinical trials [11]; its potency is similar to the antiangiogenic tyrosine-kinase inhibitor pazopanib, and lower than the multi-targeted tyrosine-kinase inhibitors sunitinib and sorafenib discontinued from cancer trials due to excessive toxicity (Fig. 8a–c; Supplementary Table 1) [50]. The gene discussed is PLG; the disease is cancer.