A 58-year-old man with poorly controlled hyperlipidaemia and smoking history presents with acute anterior wall myocardial infarction. Coronary angiography reveals plaque rupture with superimposed thrombosis in the left anterior descending artery. Histopathological examination of the ruptured plaque shows a thin fibrous cap overlying a large necrotic lipid core, with abundant lipid-laden macrophages (marked **B** in the diagram). These foam cells accumulated lipid through a mechanism that differs fundamentally from the classical LDL receptor pathway. Which of the following best explains why foam cells in atherosclerotic plaques continue to accumulate cholesterol despite high intracellular cholesterol levels?