It was shown in a trinitrobenzene sulfonic acid (TNBS) and dextran sodium sulfate (DSS)-induced colitis model that overexpression of elafin led to restoration of proteolytic balance; downregulation of IL-6, IL-8, IL-17A, and NFκΒ; and inhibition of TNF-α–induced increased permeability [32]. The gene discussed is IL17A; the disease is colitis.