We transfected LV-shFTL into THP-1-induced macrophages and RAW264.7 macrophages to specifically knock down the expression of FTL in macrophages and found that FTL could promote M2 macrophage polarization, and that FTL inhibition could reprogram tumor-promoting macrophages by inhibiting M2 macrophage polarization, thus inhibiting the glioma progression, suggesting that targeting FTL might become a promising immunotherapy strategy for glioma. This evidence concerns the gene FTL and neoplasm.