Interestingly, engineered ApoM with long plasma half-life (about 90 h) and the potential to bind S1P (such as ApoM-Fc) was when intraperitoneally administered to the experimental model of stroke in mice, an increase in plasma S1P concentration by 30% was recorded post 24 h with protection from myocardial damage after ischemia, together with reduction of hypertension and brain infarct volume compared to the control ApoM of comparable half-life with no S1P binding ability (ApoM-Fc-TM) (Swendeman et al., 2017). The gene discussed is APOM; the disease is brain infarction.