Treatment of mice with experimental autoimmune encephalomyelitis with 3,3′-Diindolylmethane (a plant-derived anti-inflammatory compound), induced the upregulation of miR-16 in brain CD4+ T cells and suppressed BCL-2; consistently, miR-16 overexpression in mouse CD4+ T cells downregulated BCL-2 (43). Here, CD4 is linked to experimental autoimmune encephalomyelitis.