Genetic studies revealed that homozygous or biallelic loss-of-function variants in LPL or its partners (GPIHBP1, APOC2, LMF1, APOA5) severely impair the efficiency of triglyceride hydrolysis, causing lifelong severe hypertriglyceridemia—the familial chylomicronemia syndrome (Dron and Hegele, 2020). The gene discussed is LPL; the disease is hypertriglyceridemia.