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To date, CNDD has been associated with biallelic variants in three kynurenine pathway genes:\n                  <jats:italic>KYNU, HAAO,<\/jats:italic>\n                  and\n                  <jats:italic>NADSYN1<\/jats:italic>\n                  . We identified two sisters with congenital anomalies overlapping with CNDD who have biallelic variants in a gene encoding a different kynurenine pathway enzyme,\n                  <jats:italic>KMO<\/jats:italic>\n                  . The surviving child also has elevated levels of metabolites upstream of KMO with low NAD\n                  <jats:sup>+<\/jats:sup>\n                  levels in plasma, suggesting that KMO deficiency is a novel CNDD. To explore the pathogenicity of KMO deficiency, we generated a global\n                  <jats:italic>Kmo<\/jats:italic>\n                  knockout mouse model (\n                  <jats:italic>\n                    Kmo\n                    <jats:sup>-\/-<\/jats:sup>\n                  <\/jats:italic>\n                  ) and utilized dietary interventions to better model human gene \u00d7 environment interactions. Although\n                  <jats:italic>\n                    Kmo\n                    <jats:sup>-\/-<\/jats:sup>\n                  <\/jats:italic>\n                  mice are viable and fertile on typical breeder chow, they exhibit elevated serum kynurenine and are functionally vitamin B3-dependent. Under conditions of limited maternal vitamin B3 intake, a greater proportion of\n                  <jats:italic>\n                    Kmo\n                    <jats:sup>-\/-<\/jats:sup>\n                  <\/jats:italic>\n                  embryos develop congenital anomalies and have significantly lower NAD\n                  <jats:sup>+<\/jats:sup>\n                  levels than\n                  <jats:italic>\n                    Kmo\n                    <jats:sup>+\/-<\/jats:sup>\n                  <\/jats:italic>\n                  littermates. Exploratory untargeted metabolomics performed in\n                  <jats:italic>\n                    Kmo\n                    <jats:sup>-\/-<\/jats:sup>\n                  <\/jats:italic>\n                  embryos suggested that NAD\n                  <jats:sup>+<\/jats:sup>\n                  deficiency may perturb the pyrimidine, purine, and pentose phosphate pathways. These findings establish KMO deficiency as a new cause of CNDD and highlight a critical gene \u00d7 environment interaction influencing NAD metabolism and congenital anomalies.\n                <\/jats:p>","DOI":"10.64898\/2026.08.24.26360911","type":"posted-content","created":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T22:35:16Z","timestamp":1787870116000},"source":"Crossref","is-referenced-by-count":0,"title":["Biallelic Variants in\n                  <i>KMO<\/i>\n                  Cause a Novel Form of Congenital NAD Deficiency"],"prefix":"10.64898","author":[{"given":"Nathalie M.","family":"Aceves-Ewing","sequence":"first","affiliation":[{"name":"Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nanbing","family":"Li-Villarreal","sequence":"additional","affiliation":[{"name":"Department of Integrative Physiology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 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