Moreover, previous studies have found that overexpression of ADAM9, induced by ROS, could increase the shedding of several membrane proteins (EphB4, Tie‐2, CD40, VCAM, Flk‐1 and VE‐cadherin) from endothelial cells to enhance pathological neovascularization33 and that ADAM9 could up‐regulate VEGFA, ANGPT2 and PLAT to promote vascular remodelling in lung cancer cells.34 We believe that ADAM9, the most representative gene for green module, could significantly participate in promoting angiogenesis in the MES GBMs and could serve as a potential therapeutic target. The gene discussed is EPHB4; the disease is lung carcinoma.