Indeed, 2 recent reports identified the critical role of EL in mediating LDL-C lowering by an LDLR independent pathway.10,11 These studies, in mice lacking both LDLR and EL, support the importance of the ANGPTL3/EL pathway in mediating VLDL remnant particle clearance and LDL-C lowering.10 The marked increase in IDL apoB FCR observed in our patients with hoFH after treatment with evinacumab are in line with those results. The gene discussed is LDLR; the disease is homozygous familial hypercholesterolemia.