The abundance of LPC and LPA under hyperlipidemic states inferred that LPC was a pro‐atherosclerotic factor and LPA was associated with coronary heart disease, including AMI.[15] Exogenous LPC/LPA resulted in elevated intracellular MPO and CitH3 levels in a concentration‐dependent manner (Figure 5C), which indicated increased activation of NETing neutrophils by these metabolites. The gene discussed is MPO; the disease is coronary artery disorder.