Of note, the latest observations on atherosclerosis in SLE patients with coexisting APS showed that atherosclerotic plaques are infiltrating by T helper (Th) cells secreting IL-17 and interferon (IFN)-γ in response to β2-GPI and suggest that β2-GPI drives a local Th17/Th1 inflammatory response, which can be responsible for plaque instability and rupture, leading to atherothrombosis [51]. The gene discussed is IL17A; the disease is autoimmune polyendocrinopathy.