These findings supported the possibility that increased Mp burden observed in the CC16-/- mice and MTECs may be due to decreased pulmonary epithelial-driven antimicrobial responses (9). A better understanding of how CC16 mediates epithelial-driven antimicrobial responses and how this regulation aids in the resolution of pulmonary infections is of paramount importance given that several patient populations have been described as having low CC16 levels, including asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis patients (10–14). Here, PPP1CB is linked to chronic obstructive pulmonary disease.