Disruption of this proposed SMAD2/3, AC061979.1, and possibly the FOXA2 ribonucleoprotein and chromatin interaction network at the MUC5B promoter by rs35705950, for example, due to aberrant splicing, could explain MUC5B overexpression in IPF, given the pivotal role of SMAD proteins in resolving goblet-cell metaplasia and hyperplasia in inflammatory pulmonary disease [56]. Here, MUC5B is linked to idiopathic pulmonary fibrosis.