In a recent study using hyperlipidemic ApoE-deficient mice, infection with Porphyromonas gingivalis and multiple microbial experimental infections (Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum) resulted in the enhanced oxidative stress response generated within aortic endothelial cells, induction of toll-like receptor (TLR) and inflammasome signaling [12]. The gene discussed is APOE; the disease is infection.