CCL2 has been shown to play crucial roles in breast and prostate tumor progression by facilitating cancer cell proliferation and survival, recruiting macrophages, and inducing angiogenesis through multiple mechanisms, including increasing survivin expression by activation of PI3K/AKT pathway and direct induction of vascular endothelial growth factor-A (VEGF-A) through activation of p42/44 mitogen-activated protein kinase (MAPK)12–15. This evidence concerns the gene VEGFA and cancer.