Except for rendering patients vulnerable to lung infections, however, the aberrant inflammation caused by PDLIM2 repression may also contribute to COPD, ILD/IPF lung disease progression, as suggested by the association of PDLIM2 repression with the severity of COPD, ILD/IPF in humans and the excessive lung inflammation and damage caused by myeloid PDLIM2 deficiency in mice treated with LPS, which in COPD, ILD/IPF may also cause disease progression. This evidence concerns the gene PDLIM2 and idiopathic pulmonary fibrosis.