Separate administering specific inhibitors of mammalian target of rapamycin (mTOR) and NF-κB pathways, such as rapamycin and BAY11–7082, to block each key nodal pathway showed that tumor-secreted CTSK combined with TLR4 via the mTOR-dependent pathway stimulates TAMs to polarize toward M2 phenotype. This evidence concerns the gene MTOR and neoplasm.