Therefore, irrespective of thyroid hormone levels, an increased TSH availability may reduce either LDLR-mediated LDL-C uptake or SREBP2-induced bile acid synthesis in hepatocytes, resulting in hypercholesterolemia, whereas a reduced TSH availability may result in hypocholesterolemia by promoting an increased hepatic expression of LDLR and activation of SREBP2. Here, SREBF2 is linked to familial hypercholesterolemia.