Theoretically, this observation would suggest the existence of (at least) two distinct pathogenetic pathways leading to alveolar injury in IPF: one involving bacterial overload in non-carriers of the MUC5B rs35705950 mutant variant and another in which carrying the MUC5B rs35705950 T allele and MUC5B overexpression at the distal airway/alveolar junction results in increased local exposure or aberrant cellular responses to bacterial stimuli [31]. Here, MUC5B is linked to idiopathic pulmonary fibrosis.