On the other hand, by adopting another subcutaneous CCA tumor mouse model with FRH0201 cells, which were shown to express a lower level of TTN-AS1 (Fig. S2A), we demonstrated that exogenous overexpression of TTN-AS1 promoted tumor growth by promoting in situ cell proliferation and tumor angiogenesis, while miR-320a mimics partially abolished these effects (Supplementary Fig. S11). The gene discussed is TTN-AS1; the disease is cholangiocarcinoma.