Moreover, TSA- or 5-AZA-dc+TSA-related upregulation of expanded chondrocytes in this report affected other genes involved in pathophysiological remodeling and inflammation, such as those encoding for ADAMTS1 and ADAMTS15 aggrecanases [38], and STAT1, a transcription factor which inhibits chondrocyte maturation in the growth plate [19] and indirectly leads to severe chondrodysplasias [39]. This evidence concerns the gene STAT1 and chondrodysplasia.