Finally, lower levels of complement C3 in viral-induced ALF followed by a high frequency of C3a, C5a, and C5b/9 deposition in the dysfunctional liver parenchyma combined with higher HepG2 susceptibility suggest that therapies targeting the complement pathway should be further investigated to control liver regeneration/damage in fulminant hepatitis caused by viral hepatitis. The gene discussed is C5; the disease is animal viral hepatitis.