Given the previous evidence showing that loss of β1,6-branched N-glycans in CD4+ T cells has an impact on the TCR signaling and T cell function,16,18,21 we analyzed the impact of this glycosylation alteration in CD4+ T cell-producing cytokines, namely IL-6 (one of the key cytokines in the etiopathogenesis of IIM). The gene discussed is IL6; the disease is acquired idiopathic inflammatory myopathy.