In the present study, we used cigarette smoke extract (CSE) - induced in vitro model of ER-stress to demonstrate that HDAC inhibition by SAHA, Tubacin (a specific HDAC6 inhibitor) or HDAC6-knockdown, controls CSE-induced ER-stress (Additional file 1: Figure S1A and B) and resulting inflammatory response, verifying its added pharmacological potential in controlling the CF-lung disease. Here, HDAC6 is linked to lung disorder.