This has clear implications for age‐related macular degeneration (AMD), a common eye disease with strong links to oxidative stress and complement activation, and for which loss of FHR‐3 deletion is protective,46 although again, the underlying mechanism requires further investigation, to determine whether the effects of FHR‐3 are entirely C3‐dependent, to verify whether intracellular or extracellular C3 activation is occurring within the RPE, and by which mechanism C3 may be being cleaved, and C3a generated. The gene discussed is CFHR3; the disease is age-related macular degeneration.