In prion disease models, activation of the signal transducer and activator of transcription (STAT)- and Nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) pathways have been observed, correlated to the up-regulation of STAT- and NFkB-responsive genes, including many cytokines and chemokines, as well as by the detection of increased phosphorylation of STAT1 and STAT3 specifically[49]. The gene discussed is SOAT1; the disease is prion disease.