Calpains can bind proline (P), glutamate (E), serine (S), and threonine (T), dubbed PEST domains, and promote degradation of IκBα by the calmodulin-like domain of the large subunit17; indeed, calpeptin attenuates CS-induced pulmonary inflammation by suppressing calpain/IκBα signaling in mice and BEAS-2B cells18. The gene discussed is NFKBIA; the disease is inflammatory response.