Previous reports have shown that C/EBPα, -β and – δare redundant for lipopolysaccharide-induced cytokine production [26,27] and the lack of effect of C/EBPδ deficiency on pulmonaryfibrosis may thus result from some kind of redundancy between family members.Using in silico analysis of publically available GEOdatasets of IPF mRNAexpression data, we identified C/EBPβ to be the most likely candidate forthe compensatory loss of C/EBPδ. This evidence concerns the gene PPIB and idiopathic pulmonary fibrosis.