Research suggests that infection with classical swine fever virus (CSFV) activates the NF-κB pathway by promoting the expression of H2B Kla and H2B K16la through the LDHA–lactate axis and that H2B K16la mediates p65 nuclear translocation through KPNA2, induces IFN-λ expression and inhibits CSFV replication [30]. The gene discussed is H2BC21; the disease is infection.