With our data showing that KRAS wild-type patients with high densities at baseline of Ang-2, CC3 and CA9 benefit from vanucizumab treatment, we hypothesise that in this ‘Ang-2-rich’ group of patients the added inhibition of Ang-2 is more effective in slowing tumour growth and metastasis than VEGF inhibition alone, counteracting tumour escape mechanisms, thus allowing increased levels of vessel normalisation and immune cell infiltration, by upregulation of the expression of adhesion molecules to which T-cells bind in order to cross the endothelial cells layer (49, 50). This evidence concerns the gene KRAS and neoplasm.