As shown in Figure 5(a), IL-19 treatment induced disruption of lung structure and collagen deposition in wild-type mice, while the extent of lung fibrosis (Figure 5(b)), lung hydroxyproline content (Figure 5(c)), and the expression of α-SMA (Figure 5(d)) were also higher than that in control groups. The gene discussed is ACTA1; the disease is pulmonary fibrosis.