To investigate the role of acetyl-CoA metabolic alteration in ICC, we firstly evaluated the expression level of acetyl-CoA hydrolysis gene ACOT12 across cancers with tumor and normal samples from the TCGA public database, and found that ACOT12 down-regulated most significantly in ICC (Fig. 1A, B). The gene discussed is ACOT12; the disease is intrahepatic cholangiocarcinoma.