Small menagerie of complement proteins can activate the complement system via classical, lectin and alternative pathways, converging on the critical complement component C3, to generate C3a, C5a and membrane-attacking complex (MAC) C5b-C9, acknowledged in the drusen of AMD patients (Crabb et al., 2002; Mullins et al., 2014; Kim et al., 2020). This evidence concerns the gene C3 and age-related macular degeneration.