Additionally, several interactions were established around the members of the immune-oncogenic gene signature and TP53, BRCA1, and AURKA, which involved in regulating spindle assembly and the cell-cycle [21], and TGF-β signaling [22], thus supporting the potential of CDK inhibitors against the immune-oncogenic related pathways behind the high-risk CCA phenotype (Figure 4c and Figure 5c). This evidence concerns the gene TP53 and cholangiocarcinoma.