BCL2 and cholangiocarcinoma: SAHA/Parthenolide combination promoted GSH depletion, Δψm reduction, and cytochrome c release and activated Caspase‐3 via histones H3 and H4 hyperacetylation or downregulated DNMT1 expression.25 SAHA and 5‐FU synergistically inhibited the proliferation of hepatocellular carcinoma cells by inducing G0/G1 arrest and caspase‐dependent apoptosis.24 Cisplatin and SAHA dose dependently and synergistically reduced the viability of cholangiocarcinoma cells and induced cell apoptosis, accompanied by upregulation of p53 and p21 and downregulation of CDK4 and Bcl‐2.22