One report described correcting the Z form of AAT secretion in response to treatment with the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) which restored Z-AAT secretion and serpin activity to 50% of wild-type AAT levels, thus suggesting that SAHA may be a potential treatment for AATD [96]. The gene discussed is SERPINA1; the disease is alpha 1-antitrypsin deficiency.