The upregulation of miR-101a is consistent with the previous finding that miR-101a is upregulated in CD4+ T cells from sanroque mice, which develop lupus-like autoimmune syndrome as a result of loss of Roquin mediated-repression of the inducible T-cell co-stimulator (ICOS)[39]. This evidence concerns the gene ICOS and systemic lupus erythematosus.