The findings for LPL and ANGPTL4 confirm recent results for two other regulators of LPL activity, APOA5 and APOC3, in that rare APOA5 mutations increase both plasma triglyceride levels and risk of CAD (Do et al, 2015), whereas rare loss‐of‐function mutations in the APOC3 gene have opposite effects (The TG and HDL Working Group of the Exome Sequencing Project, National Heart, Lung, and Blood Institute, 2014). Here, LPL is linked to coronary artery disorder.