Of interest, CD28 and NFATc1, two crucial molecules involved in T cell activation and expansion, were target genes of miR-145, and the miRNA overexpression in AChR-specific CD4+ T cells suppressed NFATc1 and IL-17 expression, thus suggesting miR-145 deficiency as a mechanism contributing to abnormal T cell activation and pathogenic Th17 response in MG [96]. This evidence concerns the gene IL17A and myasthenia gravis.