The data (mean ± SD of triplicate samples) shows that CSE induced ER-stress activity (p < 0.05) is significantly controlled by Class II HDAC inhibitor, (SAHA), selective HDAC6 inhibitor (Tubacin, B-upper panel) and HDAC6 shRNA (B-lower panel) suggesting the therapeutic potential of selective HDACi in controlling CF-related ER-stress response. This evidence concerns the gene HDAC6 and cystic fibrosis.