During anaphylaxis, crosslinking of macrophage FcγR activates macrophages to release platelet-activating factor, an endogenous phospholipid mediator that may contribute to anaphylaxis-related STEMI by inducing platelet aggregation, endothelial dysfunction, inflammatory cell adhesion, and vascular hyperpermeability (Gill et al., 2015). This evidence concerns the gene FCGR2A and anaphylaxis.