Interactions between chemokines and their corresponding receptors in the tumor microenvironment can activate several key signalling cascades, including the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) pathway, the extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway, and the nuclear factor-kappa B (NF-κB) pathway [7,33,34]. The gene discussed is MTOR; the disease is neoplasm.