While the lack of alterations in AF with the loss of Fc-receptor- or TREM2-mediated phagocytosis indicates that those particular pathways are not key contributors, AF accumulation may still be impacted by alternative phagocytic pathways active in microglia that were not tested in this study, such as TAM (Tyro3, Axl, Mer) (Fourgeaud et al., 2016; Tufail et al., 2017), SIRPα-CD47 (Hutter et al., 2019) and C3-CD11b (Fu et al., 2012; Schafer et al., 2012). The gene discussed is C3; the disease is atrial fibrillation.