Further supporting the role of TLR2, employing cells isolated from carotid endarterectomies of patients with atherosclerosis, inhibition of TLR2 and MyD88, which mediates signals for all TLRs except TLR3, suppressed the expression of spontaneously expressed inflammatory mediators and matrix metalloproteinases [16]. The gene discussed is MYD88; the disease is atherosclerosis.