In the CNS it is considered a primary effector of neurogenic inflammation in migraine [233], but has also been found to ameliorate EAE severity during disease induction through a complex regulation, in microglial elements, of the expression of proinflammatory immune activation markers, such as IL1-β and IL6, or anti-inflammatory markers, such as Ym1 and CD163 [226]. The gene discussed is CD163; the disease is migraine disorder.