More than a decade after the discovery of a novel type 1 diabetes risk locus on chromosome 16p13, there remains complexity and controversy over the specific gene(s) that regulate diabetes pathogenesis. A new study by Nieves-Bonilla et al. shows that one of these genes, DEXI, is unlikely to contribute to type 1 diabetes pathogenesis and positions the endolysosomal E3 ubiquitin ligase CLEC16A as the primary culprit by which this gene locus influences diabetes risk.

中文翻译：

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阐明1型糖尿病中16p13染色体基因的功能：CLEC16A和DEXI。

在染色体16p13上发现新的1型糖尿病风险基因位点十多年后，对于调节糖尿病发病机理的特定基因仍然存在复杂性和争议性。Nieves-Bonilla等人的一项新研究。结果表明，这些基因之一DEXI不太可能导致1型糖尿病的发病，并将溶酶体E3泛素连接酶CLEC16A定位为该基因位点影响糖尿病风险的主要元凶。