Whereas the Janus kinase (JAK)-signal transducer of activators of transcription (STAT) pathway (JAK-STAT) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) are usually activated by cytokine cascades, TLR-4, another major component of inflammation leading to atherosclerosis, is primarily activated by bacterial byproducts, more specifically by LPS [33]. This evidence concerns the gene NFKB1 and atherosclerosis.