While initially designed to prune the tumour vasculature,122–124 current clinical trials explore whether VEGF-blockade can improve immunotherapy by normalizing the tumour vasculature.125 The success of VEGF-blockade therapy is however tampered by insufficient efficacy and resistance.126,127 Several resistance mechanisms have been proposed, ranging from alternative growth factor signalling to other modes of tumour vascularization, such as vessel co-option,128,129 but only recent studies explored additional mechanisms at the single EC level.53,130. Here, VEGFA is linked to neoplasm.