Due to the interesting finding regarding APOA1 and our previous evidence regarding the contribution of dysregulated lipid metabolism in fibrotic processes and in IPF development [20,26], we also decided to test apolipoprotein E (APOE) in BALF and serum samples, in light of apolipoproteins involvement with dependent pathways aimed at modulating normal lung health and the pathogenesis of respiratory diseases, including asthma, acute lung injury, cancer, emphysema, pulmonary fibrosis, and pulmonary hypertension [27]. This evidence concerns the gene APOA1 and pulmonary fibrosis.