It is likely that subjects with low levels of various PUFAs and their products: PGE1, PGI2, PGI3, lipoxins, resolvins, protectins, and nitrolipids are not only vulnerable to develop CHD but also have poor outcome and higher incidence of cardiac failure, arrhythmias, and recurrence of myocardial infarction (Figure 1) since these endogenous lipid molecules have anti-arrhythmic action, enhance wound healing and suppress inflammation [45-49], though some studies disputed the anti-arrhythmic action of PUFAs [50,51]. The gene discussed is CD59; the disease is coronary artery disorder.