HDAC2 and chronic obstructive pulmonary disease: Sirtuins also play a crucial role in deacetylating H3K56 in mammalian cells [46,48], suggesting that in diseases such as COPD, where there is a decrease in HDAC2 [49] and SIRT1 (NAD+-dependent protein/histone deacetylase) [50–52] expression, the decreased protection against DNA breakage and repair can be explained together with the increase of somatic mutations.