A previous study has demonstrated that expression levels of AANAT and ASMT are downregulated in human CCA line Mz-ChA-1 cells compared to human normal cholangiocyte line H69 cells, and melatonin treatments inhibited Mz-ChA-1 cell proliferation and decreased tumor size in xenograft mice by inducing apoptosis in CCA cells, supporting the melatonin-mediated autocrine regulation of cholangiocytes or CCA cells [39]. The gene discussed is ASMT; the disease is cholangiocarcinoma.