Furthermore, miR-598, miR-10a, and miR-9 were significantly upregulated in both TR-AMs and Mo-AMs following BLM and potentially targeted a group of DEG shared by TR-AMs and Mo-AMs, such as Arg2, Casp8, Ccne2, Dusp6, Eif4e, Gstm1, H3f3a, Lepr, Mdm2, Prkar1b, and Ywhah. These shared DEG are involved in multiple signaling pathways that are associated with the pathogenesis of lung fibrosis, including G1/S checkpoint regulation, Myc-mediated apoptosis, clathrin-mediated endocytosis, ERK/MAPK, and PI3K/AKT signaling pathways. Here, PRKAR1B is linked to Bloom syndrome.