LPL and hypertriglyceridemia: Recently, GPIHBP1 has been recognized as the protein on the endothelial cell surface that binds LPL and facilitates TG lipolysis in the peripheral tissues (adipose tissue, heart and skeletal muscle).[27] Loss of function mutations in GPIHBP1 result in impaired lipolysis capacity leading to severe hypertriglyceridemia [17, 28–30].