Since the function of Aβ1-42 has been evoked in MS pathogenesis without definitive results [37], [38], it is reasonable to hypothesize that the P7B2 upregulation observed during the earliest (and potentially more inflammatory) MS courses might represent a cellular protection from the neurotoxicity of Aβ proteins, and that this function is reduced during the disease progression consistent with the decreased protein signal. The gene discussed is SCG5; the disease is myeloid sarcoma.