Moreover, as in CuFi-1 cells, iPA increased significantly IκBα expression (Fig. 4b) at all time points both in the presence or absence of TNFα treatment, thus indicating that iPA can act by negative modulating key inflammatory proteins involved in the NFκB and STAT3 pathways, even though the iPA-induced effect is quite different in CF and non-CF cells. Here, NFKB1 is linked to cystic fibrosis.