Utilizing both in vitro and in vivo models of CCA, herein we demonstrate that CA3, a YAP‐TEAD inhibitor, demonstrates a strong inhibitory effect on YAP‐TEAD transcription, is associated with a decrease in TEAD levels, and can arrest tumor growth in an FGFR2‐fusion patient‐derived xenograft (PDX) model of CCA. Here, FGFR2 is linked to cholangiocarcinoma.