HDAC1 and HDAC3 levels were markedly downregulated in the WD+EA group compared with the WD group (p < 0.01 and p < 0.001, respectively, Figures 3B,C), suggesting that EA treatment inhibited HDAC1 and HDAC3 overexpression after WD-TBI. The gene discussed is HDAC1; the disease is Wilson disease.