The hypercholesterolemia is actually explained by evidence that FXR activation inhibited phosphorylation levels of jun N-terminal kinase (JNK) to elevate mRNA levels of ABCG5, ABCG8, and scavenger receptor B1 (SR-B1) levels through HNF4α elevation, resulting in increased HDL uptake into the liver [104,105]. This evidence concerns the gene MAPK8 and Hypercholesterolemia.