Genetic deletion or pharmacological inhibition of STAT6 facilitated the development of potent anti-tumor immunity based on decreasing M2 macrophage polarization, demonstrating that STAT6 in CD11b+ cells promoted lung cancer progression by increasing M2 myeloid cells in STAT6−/− mice, and the mobilization and differentiation of CD11b+ cells into M2 macrophages were decreased. Here, STAT6 is linked to neoplasm.