These anti-inflammatory properties of BROM are attributed to various mechanisms, including decreased plasma fibrinogen levels, reduced bradykinin activity, increased serum fibrinolytic activity, decreased levels of prostaglandin E2 (PGE2) and thromboxane A2 (TXA2), and the modulation of adhesion molecules, such as intercellular adhesion molecule -1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-, P- and L-selectin (endothelial-, platelet- and leukocyte-selectin), CD44, and integrins (α4β1 and αLβ2) on immune cell surfaces involved in the pathogenesis of RA [172,173,174,175,176]. This evidence concerns the gene ICAM1 and rheumatoid arthritis.