Specifically, the major findings include (a) CCA cell lines are sensitive to CA3 demonstrating a decrease in TEAD levels, (b) FGFR2 fusion CCA and gastric cancer models are sensitive to CA3, (c) exposure to CA3 is associated with upregulation of an AR regulated transcriptional program, and (d) CA3 can synergize with AR inhibition to improve cancer cell killing. The gene discussed is AR; the disease is cholangiocarcinoma.