Differential expressions of these genes based on a log2 fold change cutoff of 1.5 and P < 0.05 showed an upregulation of classical profibrotic genes, including α-SMA (ACTA2), collagen 1A1 (COL1A1), collagen 3A1 (COL3A1), and collagen 6A2 (COL6A2), in IPF versus control ROIs (Figure 1, C–G). This evidence concerns the gene ACTA2 and idiopathic pulmonary fibrosis.