Nonetheless, inhibition of HDAC1, 2 and 3 by entinostat (Figure 2A) in LPS/IFN-γ induced macrophages in a COPD mouse model led to increased acetylation of NF-κB, increased translocation towards the anti-inflammatory IL-10 promoter and subsequent increased expression of IL-10 [82]. This evidence concerns the gene NFKB1 and chronic obstructive pulmonary disease.