Additionally, the release of several cytokines in GBS (tumor necrosis factor-α, interleukin-6, interferon-γ, and IL-17) (29) responsible for systemic immune activation, which, in our hypothesis, could lead to endothelial dysfunction and altered vascular permeability, is seen in PRES (3). This evidence concerns the gene IL17A and Posterior Leukoencephalopathy Syndrome.