This binding pose aligns well with data from HDX-MS analyses (Mysling et al., 2016a) and site-directed mutagenesis (Beigneux et al., 2011; Voss et al., 2011)—and it explains why certain genetic variants of GPIHBP1 and LPL are associated with hypertriglyceridemia (Henderson et al., 1996, 1998; Surendran et al., 2012; Buonuomo et al., 2015; Pingitore et al., 2016) as they compromise the complementarity of the binding interface. This evidence concerns the gene LPL and hypertriglyceridemia.