For example, mutations of the mechanistic target of rapamycin (mTOR) or platelet-derived growth factor receptor (PDGFR) occur [60], leading to tumor recurrences through a “molecular resistance.” Cooperation between EGFR and EGFRvIII induces macrophage infiltration via elevated chemokine CCL2 (CC-chemokine-ligand-2) [24]. The gene discussed is EGFR; the disease is neoplasm.