Applying the full multi-omics workflow to all recurrent, pathogenic variants highlighted MAP2K1, FLNC, TUBB3, and ABCA1 as the most compelling driver candidates; we therefore integrate our structural, epigenetic and transcriptomic findings with the mechanistic and clinical literature for each gene to delineate their individual and collective contributions to CCA pathogenesis. This evidence concerns the gene ABCA1 and cholangiocarcinoma.