Administration of the TLR4 ligand LPS into ApoE-/- mice or hypercholesterolemic rabbits promoted atherosclerosis [54, 55] and intraperitoneal administration of a synthetic TLR2/TLR1 agonist, Pam3 CSK4, increased atherosclerosis in LDLr-/- mice [53]. The gene discussed is APOE; the disease is atherosclerosis.