The activation of JNK is known to up-regulate the expression of inflammatory cytokines (IL-1, IL-6, and TNF-α) and chemokines (CCL2 and CCL5), leading to chronic inflammation and tumor initiation [39]; therefore, JNK, a representative inflammatory kinase, is strongly suggested to be one of the key players in tumor initiation. This evidence concerns the gene CCL5 and neoplasm.