The knockdown of miR-181a enhanced the production of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-8) (Hutchison et al. 2013), and increased levels of the anti-inflammatory cytokine IL-10 result from miR-181 over-expression (Murray 2005; de Vries 1995) in a murine stroke model. The gene discussed is IL10; the disease is Stroke.