Our previous studies illustrated that CXCL3 was up-regulated in tissues with cervical cancer and prostate cancer, and exogenous administration or overexpression of CXCL3 dramatically stimulated tumor cell malignant behaviors via the mitogen-activated protein kinase (MAPK)/ERK and phosphoinositide 3-kinase (PI3K)/ protein kinase B (Akt) pathways [10–12]. This evidence concerns the gene AKT1 and neoplasm.