A study conducted by Sun and colleagues (Sun et al., 2015) found a susceptibility of human hepatic epithelial cells to SFTSV, and in HepG2 cells, TNF-α and FasL were induced robustly up to 36- and 21-fold in 72h after infection of SFTSV, this latter finding indicates an extrinsic apoptotic pathway was fully activated in HepG2 by NF-KB signal pathway, moreover, pro-inflammatory cytokines including serum IL-6 and TNF-α dramatically increased as the severity of the disease increases, while inhibition of TLR3 expression was peripheral mDCs and monocytes in SFTS deceased cases (Song et al., 2017). The gene discussed is NFKB1; the disease is infection.