The rat insular cortex (IC) subserves the memory of conditioned taste aversion (CTA), in which a taste is associated with malaise. When the conditioned taste is unfamiliar, formation of Long-term CTA memory depends on muscarinic and beta -adrenergic receptors, mitogen-activated protein kinase (MAPK), and protein synthesis. We show that extinction of CTA memory is also dependent on protein synthesis and beta -adrenergic receptors in the IC, but independent of muscarinic receptors and MAPK. This resembles the molecular signature of the formation of Long-term memory of CTA to a familiar taste. Thus, memory extinction shares molecular mechanisms with Learning, but the mechanisms of learning anew differ from those of Learning the new.