Furthermore, Xiong and the colleagues reported that hyperacetylation of histones in the SOCS1 and SOCS3 promoters by trichostatin A, a histone deacetylase (HDAC) inhibitor was involved in the upregulation of SOCS1 and SOCS3, which suppressed the growth of CRC cells, and induced the cell apoptosis through downregulating JAK2/STAT3 signaling [39]. The gene discussed is STAT3; the disease is colorectal carcinoma.