Targeting macrophages using anti-Eotaxin or anti-Oncostatin M antibody may be more advantageous since this strategy not only hinders macrophage recruitment but also hinders their polarization into a pro-tumor M2 macrophage subpopulation, thus minimizing the chances of development of resistance due to commencement of M2-Like TAMs mediated pro-angiogenic cascades. Here, CCL11 is linked to neoplasm.