Although EBV was shown to inhibit IFN activated JAK/STAT pathways via a variety of mechanisms [175,176], abnormal activation of STAT1 and STAT3 (as defined by nuclear translocation and binding with DNA by STAT proteins) was observed very earlier in EBV-related lymphoma cell lines, as well as samples from patients with Burkitt’s Lymphoma (a malignant neoplasm of the haemopoietic system associated with EBV) [177]. The gene discussed is SOAT1; the disease is Burkitt lymphoma.