The relationship between increased frequency of Th17 cell subsets, which classically express CCR6, and CCM clinical activity is notable, since the entry of T cells in the CNS is facilitated by the choroid plexus, a region with weak blood–brain barrier and high expression of CCL20, natural ligand of CCR6 [24, 39, 40]. This evidence concerns the gene CCR6 and cerebral cavernous malformation.