Since we observed that both inhibition of BTKi and inhibition of mitochondrial respiration limited costimulatory molecule expression of normal human B cells, and since patients with MS have been reported to harbor B cells that can contribute to exaggerated pro-inflammatory T-cell responses in part through aberrant expression of costimulatory molecules [8, 18, 32], we wished to assess the impact of BTKi or inhibition of mitochondrial respiration on costimulatory molecule expression by B cells isolated from patients with MS. This evidence concerns the gene IBTK and myeloid sarcoma.