REST/NRSF in conjunction with RE1/NRSE also acts outside the nervous system as regulators and repressors.  Current research has linked RE1/NRSE activity with the regulation of the expression of the atrial natriuretic peptide (ANP) gene. An NRSE regulatory region is present in the 3’ untranslated region of the ANP gene and acts as a mediator for its appropriate expression. The protein encoded by the ANP gene is important during embryonic development for the maturation and development of cardiac myocytes.  However, during early childhood and throughout adulthood, ANP expression is suppressed or kept to a minimum in the ventricle. Thus, an abnormal induction of the ANP gene can lead to ventricular hypertrophy and severe cardiac consequences.  In order to maintain the repression of the gene, NRSF (neuron-restrictive silencer factor) or REST binds to the NRSE region in the 3’untranslated region of the ANP gene. Furthermore, the NRSF-NRSE complex recruits a transcriptional corepressor known as mSin3. This leads to the activity of histone deacetylase in the region and the repression of the gene. Therefore, studies have revealed the correlation between REST/NRSF and RE1/NRSE in regulating the ANP gene expression in ventricular myocytes. A mutation in either the NRSF or NRSE can lead to an undesirable development of ventricular myocytes, due to lack of repression, which can then cause ventricular hypertrophy. Left ventricular hypertrophy, for example, increases an individuals chance of sudden death due to a ventricular arrhythmia resulting from the increased ventricular mass.   In addition to the influence on the ANP' gene, the NRSE sequence regulates other cardiac embryonic genes, such as brain natriuretic peptide BNP, skeletal α-actin, and Na, K – ATPase α3 subunit. Hence, the regulatory activity of both NRSE and NRSF in mammals prevents not only neural dysfunctions but also physiological and phenotypical abnormalities in other non-neuronal regions of the body.