Remarkably, the described phenomena, i.e., generation of auto‐antibodies against CASPR1, and decrease in synaptic expression of CASPR1 and CNTN1 in retinal synapses, are not only common to the MOG/CFA‐induced EAE mouse model but occurred in a very similar manner also in the proteolipid protein (PLP) mouse model of multiple sclerosis (Fig 7). Here, CNTN1 is linked to multiple sclerosis.