LDLR and Fabry disease: The E∗3-Leiden mutation results in a dysfunctional protein with reduced binding to the low-density lipoprotein receptor (LDLr) which leads to impaired clearance of triglyceride- and cholesterol-rich lipoproteins (chylomicron and VLDL remnants), thereby mimicking the slow clearance observed in humans, particularly in FD patients.