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It is often assumed that ET\u20102 would mimic the actions of the more abundant ET\u20101 and current pharmacological interventions used to inhibit the ET system would also block the actions of ET\u20102. These assumptions have focused research on ET\u20101 with ET\u20102 studied in much less detail. Recent research suggests that our understanding of the ET family requires re\u2010evaluation. Although ET\u20102 is very similar in structure as well as pharmacology to ET\u20101, and may co\u2010exist in the same tissue compartments, there is converging evidence for an important and distinct ET\u20102 pathway. Specifically is has been demonstrated that ET\u20102 has a key role in ovarian physiology, with ET\u20102\u2010mediated contraction proposed as a final signal facilitating ovulation. Furthermore, ET\u20102 may also have a pathophysiological role in heart failure, immunology and cancer. Comparison of ET\u20102 versus ET\u20101 mRNA expression suggests this may be accomplished at the level of gene expression but differences may also exist in peptide synthesis by enzymes such as endothelin converting enzymes (ECEs) and chymase, which may allow the two pathways to be distinguished pharmacologically and become separate drug targets.<\/jats:p><jats:p><jats:bold>LINKED ARTICLES<\/jats:bold> This article is part of a themed section on Endothelin. 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