HDAC2 and chronic obstructive pulmonary disease: As in human COPD, in which no therapeutic modalities are able to repair pulmonary emphysematous destruction, neither the PTX nor the ROF therapy in our present study was able to mitigate the CS‐induced pulmonary damage (Lm remained unchanged) despite these PDEIs having demonstrated some anti‐inflammatory merits, that is IL‐8 expression being down‐regulated, and the HDAC‐2 activity being partially restored after 2 weeks of monotherapy with each of these PDEIs.