LDLR and neoplasm: Activation of LXR induces IDOL, which ubiquitinates LDLR, promotes lysosomal degradation, and inhibits cholesterol uptake. During cholesterol deprivation, LDLR expression is induced, enhancing cholesterol uptake; PCSK9 binds to LDLR and directs it to lysosomal degradation, reducing LDLR levels on the cell surface and subsequently decreasing LDL uptake. mTOR activation can bypass the LXR-IDOL axis, maintaining high LDLR expression, thereby promoting cholesterol uptake and tumor metabolism.