Moreover, small hepatitis B surface proteins (SHBs) in conjunction with β-2-glycoprotein I (β2GPI) upregulated the NF-κB pathway through TLR4/MyD88/IκBα signaling in SMMC-7721 cells [42], and in hepatitis C, TLR4 plays a major role in the capacity of B cells to activate T cells. The gene discussed is TLR4; the disease is hepatitis C virus infection.