A study in the Framingham Heart Study Offspring cohort showed that among 1780 individuals with 24 years of follow-up, those with higher bilirubin due to a genetic polymorphism affecting the UGT1A1 enzyme of bilirubin metabolism (the enzyme defect that leads to Gilbert’s syndrome) had approximately one-third the risk of cardiovascular events compared to wild-type carriers with normal bilirubin concentrations [17]. The gene discussed is UGT1A1; the disease is Gilbert syndrome.