Taken together, our results provide additional support for Hrh3 as a gene central to a neural reflex [22], [23], [24] controlling peripheral immune responses and EAE susceptibility, and as a positional candidate gene for Eae8. Importantly, our findings provide a functional framework uniting the immune- and neural-initiated models of MS pathogenesis, and provide insight into the mechanisms whereby gene-by-environmental stimuli may influence the long term progression and spectrum of clinical disease courses seen in MS [25]. Here, HRH3 is linked to myeloid sarcoma.