However, the presence of pathogenic antibodies triggers the “endothelial activation” via the pathophysiological crosstalk between brain macrophages, platelets, and endothelial cells, leading to a vicious circle of immune cells activation and proinflammatory mediators secretion, mostly type I IFN for SLE and RA, and tumor necrosis factor-α (TNFα) [2,3,72,73,74,75,76,77]. The gene discussed is TNF; the disease is systemic lupus erythematosus.