Given its defined role in the bidirectional translocation of LPL across the EC [16], and its ability to serve as a platform to promote lipoprotein-TG hydrolysis (it allows lipoproteins to stay bound/marginate to heart capillaries for several minutes [53, 54]), its absence in GPIHBP1 knockout mice causes robust hypertriglyceridemia even when these animals are fed a low-fat diet [16]. Here, LPL is linked to hypertriglyceridemia.