CRC cells enhance de novo fatty acid synthesis via upregulation of FASN, SCD1, and ACC, while increasing exogenous free fatty acid (FFA) uptake through overexpression of LDL receptor (LDLR), CD36, and fatty acid transport proteins (FATPs) to meet demands for membrane biosynthesis, signaling, and energy storage. The gene discussed is LDLR; the disease is colorectal carcinoma.