Moreover, relapsing patients display high levels of phospho-signal transducer and activator of transcription-3 (P-STAT-3) and low expression of suppressor of cytokine signaling-3 (SOCS-3) and exogenous leptin treatment sustains STAT3 phosphorylation only in the monocytes from relapsing patients, suggesting that LepR might play a role in the modulation of clinical relapses during MS (137). The gene discussed is LEPR; the disease is myeloid sarcoma.