Further, the molecules and pathogens discussed earlier such as OxLDL, HSPs, AGEs, and infectious agents, could upregulate NKG2D on different cell types, which in turn can activate T-cells, NK, and NKT cells and thus promote atherosclerosis; also other cell types as endothelial cells could produce pro-atherogenic factors, including cytokines (146). This evidence concerns the gene KLRK1 and atherosclerosis.