AD and AMD share many common pathological pathways including the appearance of dense, insoluble, Aβ42 peptide-enriched lesions (called drusen in AMD and called senile plaques in AD), a disruption in complement signaling including CFH loss-of-function or down-regulation, and the up-regulation of pro-inflammatory sncRNAs that include, prominently, miRNA-146a (32–35). This evidence concerns the gene CFH and age-related macular degeneration.