The overall results, including the upregulation of let-7i in the exosomes and downregulation of TGFBR1 and IGF1R on naive T cells, raised the possibility that alterations in the let-7i-IGF1R/TGFBR1 axis might underlie the autoimmune pathogenesis of MS. This evidence concerns the gene IGF1R and myeloid sarcoma.