For example, endotoxin (LPS) levels in the blood are strongly and independently associated with atherosclerosis in humans, and endotoxin injections augment atherosclerotic lesion development in animal models.5–8 Moreover, deletions of Toll‐like receptor 4 (TLR4) or its adaptor protein, MyD88, both of which play a crucial role in innate immune signaling, ameliorate atherosclerosis in mice.9–10. The gene discussed is MYD88; the disease is atherosclerosis.