Currently, available disease-modifying drugs are primarily designed to suppress pathological CNS inflammation and the clinical response and may result i.e. sequestering autoreactive T cells in lymph nodes away from CNS causing lymphopenia (fingolimod; 39), increasing expression and concentration of anti-inflammatory molecules (interferon beta; 40), altering immune cell function (glatiramer acetate, dimethyl fumarate; 41,42) or reducing in proliferation of activated T and B lymphocytes without causing cell death (teriflunomide; 43). Here, IFNB1 is linked to lymphopenia.