Anti-tumor immune responses in the context of melanoma largely follow a pattern of initial innate immune activation mediated by macrophages, granulocytes, and dendritic cells (DCs), all driving a subsequent Th1 response (as opposed to a Th2 response) characterized by activity of melanoma-specific effector CD4+, CD8+, and γδ T cells, functioning primarily through interferon gamma (IFNγ) [12,13]. This evidence concerns the gene CD4 and neoplasm.