More specifically, genes implicated are responsible for a range of phenotypes relevant to atherosclerosis, namely: (i) mounting pro-inflammatory responses via TLR-2 pathway (bioF-3 gene; P. gingivalis)15, (ii) bacterial adhesion underpinning intracellular and transepithelial invasion (fimA gene; P. gingivalis)15, (iii) degradation of intercellular adhesins facilitating bacterial invasion beyond the epi/endothelium barrier (prtH and prtP genes; T. forsythia, T. denticola)16,17, and (iv) host-defence evasion (ltxA and cdtB genes; A. actinomycetemcomitans)18. This evidence concerns the gene THRB and atherosclerosis.