In the lung tissues and purified AECs of patients with idiopathic pulmonary FB (IPF), the relative levels of miR-34a, miR-34b and miR-34c were significantly increased, the activity of p16, p21, p53, and SA-β-gal was increased, and the expression of miR-34 targets (E2F1, c-myc, and CCNE2) was downregulated, these changes stimulated the senescence of AECs, promoted myofibroblast transdifferentiation and induced IPF (Disayabutr et al., 2016; Cui et al., 2017b). The gene discussed is TP53; the disease is idiopathic pulmonary fibrosis.