The TIME of CCA is a highly complex, dynamic system comprising tumor cells, immune components, and blood vessels, among other constituents.[10] These different components interact with each other in ways that greatly affect the occurrence, development, and immune resistance of CCA,[11] which is characterized as a “cold tumor” with dense desmoplastic stroma that may secrete angiogenesis‐promoting molecules such as vascular endothelial growth factors (VEGF).[12] Thus, targeting angiogenesis is a potential anti‐CCA option and the entry point of our study. The gene discussed is VEGFA; the disease is cholangiocarcinoma.