For example, TNF/TNF-α is a pro-inflammatory cytokine that has been implicated in many aspects of the airway pathology in asthma, and anti-TNF-α has been demonstrated as a potential therapy in severe refractory asthma [23]; MIF plays important function in the immune pathogenesis of asthma via the promotion of TH2 responses, and its inhibition may be therapeutically beneficial to asthma [24]; The hub gene CLK1 has been shown significantly down regulated in alveolar macrophages by diesel exhaust particles, which can induce or aggravate pulmonary diseases including asthma [25]. The gene discussed is MIF; the disease is asthma.