Since plaques are known to progress by a repeated process of rupture (mainly asymptomatic) and healing, and some of the ruptured samples were collected up to three months after a clinical stroke or TIA, we also cannot entirely rule out an involvement of certain of the genes we have identified in the healing rather than the rupture process (although this seems unlikely to be the case for FABP4 and leptin). The gene discussed is LEP; the disease is Stroke.