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It plays a critical role in maintaining human genome stability through RNA primer removal, long\u2010patch base excision repair and resolution of dinucleotide and trinucleotide repeat secondary structures. In addition to its\n                    <jats:styled-content>f<\/jats:styled-content>\n                    lap\n                    <jats:styled-content>e<\/jats:styled-content>\n                    ndo\n                    <jats:styled-content>n<\/jats:styled-content>\n                    uclease (FEN) and nick\n                    <jats:styled-content>exo<\/jats:styled-content>\n                    nuclease (EXO) activities, a new\n                    <jats:styled-content>g<\/jats:styled-content>\n                    ap\n                    <jats:styled-content>e<\/jats:styled-content>\n                    ndo\n                    <jats:styled-content>n<\/jats:styled-content>\n                    uclease (GEN) activity has been characterized. This activity may be important in apoptotic DNA fragmentation and in resolving stalled DNA replication forks. The multiple functions of FEN\u20101 are regulated via several means, including formation of complexes with different protein partners, nuclear localization in response to cell cycle or DNA damage and post\u2010translational modifications. Its functional deficiency is predicted to cause genetic diseases, including Huntington's disease, myotonic dystrophy and cancers. This review summarizes the knowledge gained through efforts in the past decade to define its structural elements for specific activities and possible pathological consequences of altered functions of this multirole player. 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