In summary, our findings indicate that the abnormally elevated levels of miR-132 which we discovered in B cells of MS patients, contribute to their aberrant expression of pro-inflammatory cytokines (LT and TNFα) and that the molecular mechanism involved in this B cell effector cytokine dysregulation in patients with MS involves miR-132-mediated suppression of SIRT1, which could provide an attractive therapeutic target for patients with MS. The gene discussed is TNF; the disease is myeloid sarcoma.