CCA lines, Mz-ChA-1, HuH-28, and TFK-1 cells, expressed CCK-BR, and gastrin treatments decreased cell proliferation in CCA cells by inducing apoptosis via elevated inositol 1,4,5-triphosphate (IP3) secretion and protein kinase C alpha (PKC-α) expression [70]. The gene discussed is CCK; the disease is cholangiocarcinoma.