In contrast to the findings observed in the ACC and IC, neither SDS nor TR changed the expression levels of HDAC1 and HDAC2 in the RVM or C2 region; however, in a bone cancer pain model, HDAC1 and HDAC2 levels were significantly increased in the spinal cord, and inhibition of their enzymatic activity effectively reduced hyperalgesia-like behaviors in the hindpaw [58]. The gene discussed is HDAC2; the disease is bone neoplasm.