In contrast, PMS groups (but not RRMS patients) had significantly lower expression of TNFRSF1A (52) in blood leukocytes, suggesting that this is either a consequence of higher TNF-α production in progressive MS (as part of negative feedback loop), or, alternatively, lower expression of the receptor may cause lower consumption of TNF-α by immune cells derived from progressive MS. The gene discussed is TNF; the disease is premenstrual tension.