Activated DCs experience alterations in gene expression and exhibit reduced capacity for antigen uptake and processing, while they express more MHC-II, CCR7, and costimulatory molecules, such as CD40, CD80, and CD86, and undergo CCR7-dependent migration to draining lymph nodes (dLNs) or the T cell zone in the splenic white pulp, where they ingest and process tumor antigens to T cells and other immune cells, resulting in the initiation of thus triggering effective cancer-specific immune responses [9, 31, 33, 34]. This evidence concerns the gene CD86 and neoplasm.