NKT cells present in AAA tissue predominantly produce pro-inflammatory IFN-γ, which may lead to an upregulated expression of Fas and increased FasL-mediated apoptosis of vascular smooth muscle cells (vSMCs).[20] However, later on it was reported that the anti-inflammatory IL-4, produced by the same NKT cells, might be responsible for increased expression of MMPs by SMCs and macrophages, thereby possibly contributing to the development of AAA.[25–27]. The gene discussed is FASLG; the disease is triple-A syndrome.