Dalla Libera et al. [23] reported decreased numbers of Tregs (defined by CD25, Foxp3, CD39, CTLA-4, and GITR expression) in RRMS patients during remission, which were restored to normal levels in the acute phase, concluding that Tregs are not involved in causing clinical attacks, but retain functionality and are increased during acute phase to restore homeostasis. The gene discussed is CTLA4; the disease is relapsing-remitting multiple sclerosis.