ICAM1 and glioblastoma: Treatment of GBM with anti-VEGF monoclonal antibody bevacizumab for instance—currently the only FDA-approved targeted treatment for glioblastoma and one that has not been shown to have survival benefit—eventually induces STAT3 activation likely via the hypoxia response, leading to the expression of stemness and invasive markers such as nestin and ICAM-1, respectively [150].