Rached et al. [42] have reported that HDL3b subpopulations in early-phase ST segment elevation myocardial infarction are enriched in lysoPC and phosphatidic acid, depleted in ApoA1 and enriched in serum amyloid A. These changes in the HDL lipidome together with changes in the HDL proteome contributed to functional deficiencies in cholesterol efflux and antioxidative activities of the circulating HDLs in these patients [42]. The gene discussed is APOA1; the disease is myocardial infarction.