We showed that proteins that regulate cell death provide effective strategies to control the number of mucus-secreting cells in airway epithelia. These proteins not only are crucial in discarding excess mucus cells but also interact with NF-κB and regulate the activation and transcription of cytokines. Further, we found that peptides derived from these proteins reduce mucus cell numbers by causing death of these cells and also by suppressing inflammation. Genetic variants in genes encoding for these proteins and are responsible for making individuals more susceptible to chronic bronchitis and rapid decline in lung function are being studied. Also, peptides and small inhibitor molecules that efficient in reducing mucus cells are being developed to be tested in human clinical trials.