ADAM17 and idiopathic pulmonary fibrosis: Given the presence of these signals in IPF lung (Figure 3 and Figure 4), the importance of AREG and IL6 pathways in IPF [22,23,24,34,35,36,37,38], and the finding that ADAM17 signals were increased in AECI from MUC5B variants (Figure 4), we hypothesized that excessive ADAM17 signals in MUC5B variants could precipitate development of IPF.