In nonmalignant cholangiocytes and in nc886-expressing cholangiocarcinoma cells, nc886 knockdown led to up-regulation of PKR activity with two different outcomes: In nonmalignant cells, activated PKR resulted in increased eIF2α phosphorylation, decreased protein synthesis, and promoted apoptosis, whereas in cholangiocarcinoma cells, it resulted in activation of NF-κB (Kunkeaw et al. 2013). Here, EIF2AK2 is linked to cholangiocarcinoma.