It remains to be determined whether drugs that inhibit PKR activation, including C16 (Xiao et al., 2016), or compounds that disrupt PACT/PKR-mediated signaling, such as luteolin (Dabo et al., 2017), will be effective in treating diseases with inflammatory components, such as IBD (Schwartz et al., 2009), or diseases with a hyperosmotic component, such as dry eye syndrome (Lemp et al., 2011). This evidence concerns the gene PRKRA and inflammatory bowel disease.