It was demonstrated that TNF-α is apivotal player in the development of ALI, and that intranasal administration ofan aptamer targeting TNF-α, conjugated with 40 kDa polyethylene glycol(PEG-aptTNF-α), to mice with ALI suppresses the development of aninflammation in the respiratory system of experimental animals. The gene discussed is TNF; the disease is acute respiratory distress syndrome.