Furthermore, a translational trial [44] investigating the effect of short-term, high-dose atorvastatin treatment on intratumoral cholesterol homeostasis of breast cancer patients showed that, after treatment, the expression of LDL receptor (LDLR) significantly increased in response to the negative feedback activated by the cholesterol depletion caused by the block of the mevalonate pathway and aimed to supply the required level of cholesterol through increased uptake of the circulating cholesterol-rich LDL. This evidence concerns the gene LDLR and breast cancer.