The participation of proinflammatory cytokines in the progression of Multiple Sclerosis (MS) has been well documented. Cytokines activate the JAK-STAT pathway, in which the suppressors of cytokine signaling (SOCS) exert a negative feedback. This paper analyzes the levels of SOCS5 and SOCS7 transcripts, quantified by RT-qPCR, in MS patients, and the concentrations of proinflammatory cytokines, IFN-&gamma / , IL17, and IL6, determined by ELISA. Samples of peripheral blood were obtained from MS patients in the relapsing&ndash / remitting phase, treated with IFN-&beta / or glatiramer acetate (GA), and from healthy individuals. SOCS7 mRNA was significantly higher in patients treated with GA (1.36 ± / 0.23) than in those treated with IFN-&beta / (0.65 ± / 0.1). Regarding gender, the level of SOCS5 and SOCS7 transcripts were similar between MS and healthy females / in MS males, the level of SOCS7 transcripts were significantly lower (0.59 ± / 0.03) than in healthy males (1.008 ± / 0.05). Plasmatic levels of IFN-&gamma / were significantly higher in MS patients (60 pg/mL, range 0&ndash / 160) than in healthy subjects (0 range, 0&ndash / 106). The same pattern was observed in MS patients treated with IFN-&beta / (68 pg/mL, range 0&ndash / 160) compared to patients treated with GA (51 pg/mL, range 0&ndash / 114), and in MS females (64 pg/mL, range 0&ndash / 161) compared to healthy females (0, range 0&ndash / 99). We hypothesize that the increase in SOCS7 transcription in patients treated with GA could partially explain the action mechanism of this drug, while the increase in the concentration of IFN-&gamma / in MS patients could help elucidate the immunopathology of the disease.