Although the existence of an LDLR-independent pathway is supported by studies in mice8,10 as well as by the remarkable reduction in LDL-C observed in patients with hoFH treated with evinacumab19,20 and the increase in LDL apoB FCR in carriers of either LDLR null/null or defective variants observed in this study, it is not yet clear what receptor(s) are responsible for apoB-containing lipoproteins uptake from the circulation. This evidence concerns the gene APOB and homozygous familial hypercholesterolemia.