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A number of recent advances have clarified details of how metabolic pathways can specifically affect cellular function in immune cells. Critical to this understanding is ongoing study of the congenital disorders of glycosylation and other genetic disorders of metabolism that lead to altered immune function in humans. While there are a number of immune phenotypes associated with metabolic derangements caused by single gene disorders, several genetic mutations have begun to link discrete alterations in metabolism and growth specifically with allergic disease. This subset of primary atopic disorders is of particular interest as they illuminate how hypomorphic mutations which allow for some residual function of mutated protein products permit the \u201cabnormal\u201d allergic response. This review will highlight how mutations altering sugar metabolism and <jats:styled-content style=\"fixed-case\">mTOR<\/jats:styled-content> activation place similar constraints on T lymphocyte metabolism to engender atopy, and how alterations in <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content> signaling can impair growth and cellular metabolism while concomitantly promoting allergic diseases and reactions in humans.<\/jats:p>","DOI":"10.1111\/imr.12727","type":"journal-article","created":{"date-parts":[[2018,12,19]],"date-time":"2018-12-19T01:12:24Z","timestamp":1545181944000},"page":"135-144","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["The clinical and mechanistic intersection of primary atopic disorders and inborn errors of growth and 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