ADAM17 and neoplasm: It cleaves membrane‐bound precursors of pro‐angiogenic factors such as VEGF family members, releasing active ligands that rapidly activate EGFR/ERK signaling pathways in endothelial cells, thereby promoting proliferation and migration.[29, 53] Additionally, ADAM17 regulates matrix metalloproteinase activity to remodel the extracellular matrix and facilitate neovascularization.[54] Loss of ADAM17 in endothelial cells impairs their physiological function.[28, 55] Recent evidence indicates that tumor cells package ADAM17 into exosomes and release them.