In murine syngeneic and xenogeneic tumor models, BTH1677 combined with various tumor-targeting MAbs [28–31], PD-1 and PD-L1 checkpoint-inhibiting MAbs [31–33], or VEGF/VEGFR2-targeted MAbs [22, 23, 31, 34–37] has resulted in greater suppression of tumor growth and longer survival than with either agent alone. Here, VEGFA is linked to neoplasm.