This clear discrepancy between the overexpression of RAGE in UIP fibroblasts and epithelial cells and the absence of expression of its main signal transductor, in the absence of comparable literature data, can be explained with expression levels of NF-κB below the threshold of immunohistochemical detection, or with a rapid turnover that limits the amount of detectable protein. This evidence concerns the gene NFKB1 and idiopathic pulmonary fibrosis.