Such a hypothesis is in agreement with recent findings showing that anti-JAM-C treatment decreases inflammation in various mouse inflammatory models such as cerulein-induced pancreatitis, thioglycollate-induced peritonitis, or allergic contact dermatitis [11-13] and that the protein may be involved in other diseases such as obstructive nephropathy or atherosclerosis [10,33]. This evidence concerns the gene JAM3 and atherosclerosis.