Patients with hTG remain in the epicentre for the development of cardiovascular disease despite recent decades of intensified dyslipidaemia treatment.2,11–14 A Tg level >1.7 mmol/L (>150 mg/dL) constitutes residual cardiovascular risk for patients in secondary prevention on effective LDL cholesterol lowering therapy15 and in individuals with subclinical atherosclerosis regardless of their LDL cholesterol level.16 However, strategies to pharmacologically lower plasma Tg levels to reduce ASCVD events have not been straightforward. The gene discussed is TG; the disease is cardiovascular disorder.