SM patients have been found to produce greater levels of proinflammatory cytokines (e.g. IL-1β, IL-6 and TNF), than patients with uncomplicated malaria, while evidence has accumulated over the years implicating the upregulation of the inflammatory response as a contributory factor to SM pathogenesis, and malaria-associated AKI in particular (27, 28). The gene discussed is IL1B; the disease is malaria.