TBK1 and Epstein-Barr virus infection: We further revealed that the expression tendency of Gal-9, phosphorylated STAT3 (p-STAT3 - a key molecule in B-cell transformation and LCL proliferation) (14, 15), and STING signaling proteins such as the activated TBK1 were consistent with the proliferation (cluster 5 and 3) and antiviral (cluster 4) pathway models of primary B cells post-EBV infection (Fig. 1D).