In addition to dysregulation of the de novo synthesis of cholesterol, altered cholesterol influx mediated by factors such as CD36, VLDLR, LDLR, the scavenger receptor class B member 1 (SCARB‐1), ABCG1, and ABCA1,94 also contributes to cholesterol homeostasis in cancer cells through a process largely transcriptionally regulated by LXR.95 This evidence concerns the gene CD36 and cancer.