Furthermore, both H. pylori [32] and LPR [33] have been shown to induce an over-expression of CD1d in mucosal tissue, and both CD1d and lipid antigens can stimulate CD1d-restricted T cells (i.e., natural killer T cells) to further activate innate and adaptive immune cells in the tumor microenvironment [34]. This evidence concerns the gene CD1D and neoplasm.