As shown in the network, a number of revealed asthma-specific genes plays known regulatory functions in pulmonary fibrosis, such as Igf1, Spp1, and Timp1 mentioned above; mucins Muc5ac and Muc5b, playing a key role in resolving fibrosis-induced disrupted homeostasis in lungs [96]; chemokines Ccl2 and Ccl12 involved in recruiting fibrocytes and exudative macrophages in fibrotic areas [97]; as well as catalase (Cat), inhibiting fibrosis-associated mitochondrial DNA damage in alveolar epithelial cells and their apoptosis [98]. This evidence concerns the gene TIMP1 and asthma.