Mechanistically, CCL11 stimulates tumor progression through the activation of key signaling phosphoproteins (ERK1/2, MEK1, and STAT3) and the upregulation of diverse molecular mediators, including cytokine receptors (IL-6R), chemokines (MIF, CXCL8, G-CSF, GM-CSF, and M-CSF), growth/angiogenic factors (VEGF and SDF-1α), and adhesion molecules (ICAM-1). Here, MAPK3 is linked to neoplasm.