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However, it can be questioned what actually defines FCHL.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Recent Findings<\/jats:title>\n            <jats:p>Although initially regarded as an autosomal dominant disorder, quantitative trait linkage analyses have revealed multiple genes that are associated with the FCHL phenotype. With the advent of genome-wide association studies and next generation sequencing it has been confirmed that FCHL is a polygenic disorder and the associated gene variants, mostly with a triglyceride-raising effect, are not unique to FCHL. Furthermore, epidemiological studies have demonstrated that the multiple-type hyperlipidemia is also not specifically confined to FCHL.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Summary<\/jats:title>\n            <jats:p>This review provides a historical overview of the metabolic and genetic abnormalities that characterize FCHL. Integration of these findings with recent population-based, genetic studies results in a new pathophysiological concept of FCHL. This model provides practical guidance on how to approach an individual patient with an \u2018FCHL phenotype\u2019.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1007\/s11883-025-01289-9","type":"journal-article","created":{"date-parts":[[2025,4,3]],"date-time":"2025-04-03T14:19:58Z","timestamp":1743689998000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Familial Combined Hyperlipidemia: Myth or Reality?"],"prefix":"10.1007","volume":"27","author":[{"given":"M. C. G. 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