Lastly, the knock-out of MyD88, a downstream signaling molecule involved in both the TLR-2 and TLR-4 pathway, reduced both AAA formation and atherosclerosis after angiotensin II infusion in mice predisposed to both disease entities by the knock-out of either apolipoprotein E or low-density lipoprotein receptor (LDL-R) [108]. This evidence concerns the gene TLR4 and triple-A syndrome.