It has been shown in a mouse model that CC16 administration increases epithelial proliferation, protects against oxidative stress [26], and is suggested to be linked to a population of Clara cells, producing CC16 protein, with a bone marrow (BMC) phenotype which would be implicated in lung repair by reducing pulmonary inflammation and promoting airway regeneration [27]. The gene discussed is SCGB1A1; the disease is inflammation.