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Beginning with the discovery of the '''s'''terol regulatory element binding proteins (SREBPs) in 1993, a productive combination of biochemistry, molecular biology and genetics, has brought to light the complex mechanisms by which animal cells maintain the proper levels of intracellular lipid (fats and oils) in the face of widely varying circumstances (lipid homeostasis). These studies exposed a signaling mechanism of beguiling complexity that is responsible for the end-product feedback regulation of gene transcription. For example, when cellular cholesterol levels fall below the level needed, the cell makes more of the enzymes necessary to make cholesterol. A principal step in this response is to make more of the mRNA transcripts that direct the synthesis of these enzymes. Conversely, when there is enough cholesterol around, the cell stops making those mRNAs and the level of the enzymes falls. As a result, the cell quits making cholesterol once it has enough.