Regarding the relationship between miR-29 and type I collagen (COL1), Khalil et al. found that the mechanism by which miR-29 inhibition IPF fibroblasts and polymerized collagen involves the reduction in the function of protein phosphatase (PP) 2A, which leads to lessening phosphorylation of histone deacetylase 4 (HDAC4) and a reduction in the nuclear translocation of HDAC4. This evidence concerns the gene HDAC4 and idiopathic pulmonary fibrosis.