peak expression within 30 minutes after stimuli compared to 2–4 hours in the case of delayed primary response gene. There are many singaling pathways leading to the activation of IEGs, many of which (MAPK/ERK, PI3K, etc.) are studied in the context of cancer. As such, many IEGs function as transcription factors regulating expression of downstream genes or are proto-oncogenes associated with altered cell growth. Clinical significance Expression of IEGs is involved in neuronal activity and specifically memory formation, neuropsychiatric diseases, and behavioral activities. Immediate early genes present in the brain are associated with a range of functions such as modifying synaptic functions through transient and rapid activation growth factors or the expression of cellular proteins. These changes are theorized to be the means in which memory is stored in the brain as outline in the concept of memory trace or engram. In the context of neuropsychiatric diseases, up-regulation of certain IEGs related to the formation of fear-related memories contribute to the development of a variety of disease such as schizophrenia, Panic disorder, Post-traumatic stress disorder Memory formation Some IEGs such as ZNF268 and Arc have been implicated in learning and memory and long-term potentiation. A wide range of neuronal stimulation have been shown to induce IEG expression ranging from sensory and behavioral to drug-induced convulsions. As such, IEGs are utilized as a marker to understand neuronal ensembles associated with formations of certain memories such as fear, commonly attributed to the development of psychiatric disorders. For example, neurons expression Arc in the hippocampus show phenotypic and behavioral differences in response to stimuli such as altered dendritic spine morphology or spontaneous firing rate. This association suggests the expression of certain IEGs in response to a stimulus results in expansion of the related neuronal circuit by incorporating the activated neuron assembles. Other IEGs effect different neural properties with knock out of Arc showing adverse affects on the formation of long-term memory. These findings offer insight into the molecular mechanism and functional changes brought about by IEG expression, expanding the theory of memory trace. Memory consolidation during a learning experience depends on the rapid expression of a set of IEGs in brain neurons. In general, expression of genes often can be epigenetically repressed by the presence of 5-methylcytosine in the DNA promoter regions of the genes. However, in the case of IEGs associated with memory consolidation demethylation of 5-methylcytosine to form the normal base