Moreover, CD4+ TH cells derived from cured animals treated with L19mTNFα/melphalan, while fully competent in generating tumor rejection when adoptively transferred together with tumor cells in naive mice, were incapable of inducing tumor rejection in CD8-depleted naïve animals, strongly suggesting that a major protective role of primed anti-tumor CD4+ T cells lies in triggering CD8+ naive T cells to become functionally mature antitumor CTL effectors [46]. This evidence concerns the gene CD4 and neoplasm.