A strong proinflammatory Th1 and Th17 response was seen in patients with MERS, with markedly increased concentrations of proinflammatory cytokines (IFN-γ, TNF-α, IL-15, and IL-17), that elicited a type II IFN response with innate and acquired immunity interfering with viral replication [27,31]. The gene discussed is IFNG; the disease is Middle East respiratory syndrome.