NFKB1 and cholangiocarcinoma: In line with this, in CC, increased GCDA levels have been demonstrated to fuel chronic inflammation via induction of endoplasmic reticulum stress, promoting increased release of reactive oxygen species (ROS), DNA damage, and ultimately aberrating cell replication [85,86]; furthermore, reduced CDA levels have been shown to stimulate cell proliferation via interfering with EGFR/Early growth response factor 1 (EGR1)/MAPK and protein kinase C (PKC)/MAPK/NF-kB signaling [87].