MTOR and neoplasm: Li et al. discovered that, in microenvironmental disruption induced by intestinal dysbacteriosis, tumor-secreted metastasis-related secretory protein cathepsin (KCTSK) can bind to Toll-like receptor 4 (TLR4), to stimulate M2 polarization of tumor-associated macrophages (TAMs) via an mTOR-dependent pathway, which, in turn, promote the invasion and metastasis of NSCLC cells through the NF-κB pathway [50].