Igfbp2 silencing in mouse lung epithelial cells increased P21 levels and SA‐β‐gal activity in response to profibrotic stimuli, while transgenic aged mice expressing human Igfbp2 diminished senescence and profibrotic SASPs, resulting in amelioration of bleomycin‐induced pulmonary fibrosis.[67] Here, the AML12 cells overexpressing IAL‐miRs exhibited an increase in the number of SA‐β‐gal positive cells and a suppression of cell proliferation. This evidence concerns the gene IGFBP2 and pulmonary fibrosis.