Since both C10 and U18666a induce cancer cytotoxicity by disrupting cholesterol homeostasis possibly through distinct mechanisms, we sought to further differentiate these two compounds by treating cancer cells with C10 in combination with mevalonate, especially since (1) mevalonate is the product of the rate limiting step catalyzed by HMGCR in the de novo synthesis pathway of cholesterol, and (2) mevalonate supplementation was previously reported to provide significant neuroprotection to cells treated with U18666a. This evidence concerns the gene HMGCR and cancer.