These include dominant variants in LPL, APOE, APOA5, and LIPC and recessive variants in APOC2, GPI-HBP1, LMF1, APOE, and GPD1. In our NGS cohort, most pathogenic variants are located in LPL, APOA5, and APOC2. It is disputable what the role of some of these variants in disease pathogenesis is, as many of these variants only provoke dyslipidemia when secondary factors are involved, such as alcohol, diet, hormones, and other medications and secondary diseases such as diabetes and hypothyroidism [58,59]. Here, LPL is linked to metabolic syndrome.