In the present study, we investigated the following two hypotheses: 1) To determine if the signaling pathway going through the MAPKs: p38, extracellular-regulated protein kinase (ERK), and Jun-N terminal protein kinase (JNK) to the transcription factor activator-protein-1 (AP-1) signaling is dysregulated in CF epithelial cells; 2) To determine whether this pathway can be manipulated by parthenolide. Here, MAPK8 is linked to cystic fibrosis.