Cell culture experiments have shown that NPC1L1 mediates cellular uptake of various sterols but seems to have lower affinity to plant sterols than cholesterol. Transgenic animal studies have demonstrated that hepatic NPC1L1 has the potential to regulate biliary cholesterol excretion. Cholesterol and many transcriptional factors appear to regulate NPC1L1 gene expression. NPC1L1 protein is enriched in the apical membrane of polarized cells and its intracellular itineraries are clearly regulated by cholesterol availability. Also, cholesterol-regulated clathrin-mediated endocytosis is likely the cellular basis for NPC1L1-dependent cholesterol uptake, which may reconcile disagreement regarding NPC1L1 subcellular localization.

Yes, thank you

But, to be more clear in my question, how could I know, when I use a cholesterol absorption inhibitor substance, that it acts on NPC1L1 and not differently

It is also unclear how NPC1L1 modulates the pathogenesis of fatty liver disease, insulin sensitivity, and diet-induced obesity.

But, NPC1L1 may have evolved to prevent excessive loss of cholesterol from bile, likely by transporting cholesterol in the bile canaliculus back into hepatocytes. And develop a study design.