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The phenotypic manifestation and the severity of NAFLD are influenced by an interplay of environmental and genetic factors. Recently, several inactivating variants in the novel\n                      <jats:italic>17\u2010Beta hydroxysteroid dehydrogenase 13 (HSD17B13)<\/jats:italic>\n                      gene have been found to be associated with a reduced risk of chronic liver diseases, including NAFLD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>\n                      To review the existing literature on the epidemiology of\n                      <jats:italic>HSD17B13<\/jats:italic>\n                      and discuss its role in the natural history, disease pathogenesis and treatment of NAFLD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We extensively searched relevant literature in PubMed, Google Scholar,\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/clinicaltrials.gov\">clinicaltrials.gov<\/jats:ext-link>\n                      and the reference list of articles included in the review.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      HSD17B13 is a liver\u2010specific, lipid droplet (LD)\u2010associated protein that has enzymatic pathways involving steroids, pro\u2010inflammatory lipid mediators and retinol. The estimated prevalence of the best characterised\n                      <jats:italic>HSD17B13<\/jats:italic>\n                      variant (rs72613567) ranges from 5% in Africa to 34% in East Asia. Loss\u2010of\u2010function variants in\n                      <jats:italic>HSD17B13<\/jats:italic>\n                      are protective against the progression of NAFLD from simple steatosis to non\u2010alcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis and hepatocellular carcinoma. Emerging data from mechanistic and preclinical studies with RNA interference (RNAi) and small molecule agents indicate that inhibiting\n                      <jats:italic>HSD17B13<\/jats:italic>\n                      activity may prevent NAFLD progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      The loss\u2010of\u2010function polymorphisms of the newly identified\n                      <jats:italic>HSD17B13<\/jats:italic>\n                      gene mitigate the progression of NAFLD. It is important to understand the exact mechanism by which these variants exert a protective effect and implement the gathered knowledge in the treatment of NAFLD.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apt.17292","type":"journal-article","created":{"date-parts":[[2022,11,9]],"date-time":"2022-11-09T04:46:03Z","timestamp":1667969163000},"page":"37-51","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":65,"title":["Review article: the role of\n                    <scp>HSD17B13<\/scp>\n                    on global epidemiology, natural history, pathogenesis and treatment of\n                    <scp>NAFLD<\/scp>"],"prefix":"10.1111","volume":"57","author":[{"given":"Maral","family":"Amangurbanova","sequence":"first","affiliation":[{"name":"NAFLD Research Center, Division of Gastroenterology University of California at San Diego  La Jolla California 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