Moreover, administration of oral curcumin to ΔF508 CF mice, resulted in sufficient correction of ΔF508 CFTR trafficking, that normalized nasal potential-difference measurements could be attained; including a reduction in the level of epithelial sodium transport (a process which is thought to be a significant contributor to CF lung pathology) [33,34]. The gene discussed is CFTR; the disease is cystic fibrosis.