Although the way in which dimer formation contributes to NF-κB pathway inhibition is still unclear, intranasal inoculation of mice using either the ΔN1L strain or strains encoding the I6E N1 mutant were typified by reduced virulence compared to WR infections, suggesting that N1 dimerization and antagonism of NF-κB contributes to VV pathogenesis [126]. Here, NFKB1 is linked to infection.