Both TMEM16A and SLC26A9 activities which attenuate airway inflammation and prevent mucus obstruction during airway inflammation have been considered as alternative therapeutic targets to bypass CFTR dysfunction in the airway epithelia of CF patients However, strategies for increasing intracellular calcium concentration to stimulate calcium-activated chloride secretion have been plagued by the amplification of the calcium dependent pro-inflammatory response [58,59]. The gene discussed is CFTR; the disease is cystic fibrosis.