Given the relationship between cilengitide treatment and STAT3 activation observed in melanoma cells (65), we performed Western blotting experiments showing that cilengitide treatment upregulated p-STAT3 in GBM cells (Figure 7, A and B), suggesting that dual targeting of integrin αv and STAT3 is required for blocking LGMN-induced GBM biology. The gene discussed is STAT3; the disease is melanoma.