Moreover, we demonstrated that iPA was also able to slow down the NFκB pathway by increasing its direct inhibitor IκBα in both CF and TNFα-stimulated non-CF cells, thus suggesting that iPA can act as a NFκB inhibitor decreasing the production of the pro-inflammatory chemokines IL-8 and RANTES. The gene discussed is CXCL8; the disease is cystic fibrosis.