Hafner et al. (2012) reported that while PrP-fibrils were able to activate NF-κB, and increase IL-1β mRNA, this activation might not be sufficient to produce prominent amounts of pro-IL-1β protein, but could produce enough to induce a primed state, which might be easily abrogated by bacterial infections or endogenous danger signals (Combrinck et al., 2002). The gene discussed is IL1B; the disease is bacterial infectious disease.