Theaim of current study was to investigate whether 1,25(OH)2D3administration would alter the expression of HDAC2, which is involved in theGC-dependent repression of NF-κB-induced gene expression, and whether increased HDAC2expression could enhance GC responsiveness in GC-insensitive diseases such as an animalmodel of asthma. Here, HDAC2 is linked to asthma.