In addition, the upregulation of p-STAT3 would affect the treatment efficiency of VEGF-targeted anti-angiogenic agent, as anti-angiogenic therapy-mediated induction of hypoxia in the glioblastoma microenvironment can be directly activated by STAT3/HIF-1/VEGF that was associated with tumorigenesis and progression (Yuan et al., 2015). The gene discussed is VEGFA; the disease is glioblastoma.