The predominant mechanism of action of TP has traditionally been ascribed to non-selective inhibition of phosphodiesterase enzymes (Nicholson and Shahid, 1994), but there is increasing evidence that some of the clinical effects of TP might be due to other mechanisms of action such as increasing histone deacetylase enzyme(s) activity (HDAC; Ito et al., 2002), or interference with certain intracellular kinases (To et al., 2010); the latter mechanism has also been suggested to account for the ability of TP to reverse glucocorticosteroid insensitivity in patients with COPD. The gene discussed is HDAC9; the disease is chronic obstructive pulmonary disease.