Signalling pathways activated by CXCL9 and CXCL10 seem to directly contribute to prion disease progression, as suggested by the finding that scrapie infected-CXCR3 KO mice (lacking the CXCL9 and CXCL10 receptor), although exhibiting exacerbated astrocytosis and accelerated accumulation of PrPSc, showed reduced microglia activation and pro-inflammatory factor secretions, and survived longer compared to scrapie-infected WT mice [91]. The gene discussed is CXCL10; the disease is prion disease.