Considering the abundance of PAC1 receptors in the spinal cord [45] and the fact that synapse dysfunction in this structure is a commonly observed pathological feature of MS [46,47], we were interested in determining if partial or complete deletion of the PAC1 receptor gene affected the expression of both Synapsin II and Synaptophysin, two prominent pre-synaptic vesicle-associated proteins critical for synaptic transmission and plasticity, with documented synaptic loss linked to disease progression in MS and preclinical models of disease [48,49]. The gene discussed is SYN2; the disease is myeloid sarcoma.