The mechanism depicted in Fig. 1 is further supported by experiments showing that tumor inhibition in DNP-immune mice treated with VEGF–DNP was accompanied by intratumoral accumulation of immune cells with a Th1 proinflammatory signature (Supplementary Fig. 4), was FcR dependent (Fig. 4) and T cell mediated (Fig. 5). Here, VEGFA is linked to neoplasm.