In addition, a very recent paper [34], using the same CIA model, also suggests that the administration of the PKRs antagonist PC1 improved clinical signs of arthritis, lowered plasma malondialdehyde (MDA) levels, and reduced joint expression of PK2, PKRs, TNFα, IL-1β, CD4, CD8, and NF-kB. The gene discussed is PROK2; the disease is arthritic joint disease.