On the ex vivo cultures of cells isolated from human atherosclerosis plaques the production of several cytokines, inflammatory mediators and metalloproteinases was significantly reduced with dnMyD88 (MyD88 aa 53-296 P56N) [131] where the P56N mutation in the DD of MyD88 is unable to form DD homodimers [132]. This evidence concerns the gene MYD88 and atherosclerosis.