Neil3是涉及基础切除修复（BER）的DNA N-糖基酶，氧化DNA损伤的主要修复途径。Neil3可以以5-胍酰亚胺丁蛋白和螺米氨酸的形式检测和除去氧化的鸟嘌呤，并以胸腺嘧啶乙二醇的形式氧化胸腺嘧啶。Neil3具有对单链DNA（SSDNA）的偏好，并且涉及在端粒体的氧化DNA损伤修复（周等，2013）。Neil3疾病变体Neil3 D132不能从氧化受损的DNA中切割5个胍啶醛素（GH）。涉及Neil3 D132V纯合突变的个体倾向于自身免疫性疾病的发展（MassaAd等，2016）和Neil3耗尽也与端粒损坏和损失的增加有关（周等人2017）。Neil3在DNA复制期间蚕食DNA Interstrand（ICL）。Neil3在FANCONI贫血（FA）途径（SEMLOW等人2016中，Martin等人2017）中解析了PSORALEN-和ABASIC网站诱导的ICLS（Martin等，2017）。NEIL3基因剪接部位之一的多态性可能会增加风险心肌梗死（Skarpengland等，2015）。心脏病在人类心力衰竭和小鼠疾病模型中心肌梗死后的心力衰竭后，Neil3表达增加。Neil3敲除小鼠显示心肌梗塞后的死亡率增加，但Neil3敲除心脏的DNA损伤没有增加。 In the heart, NEIL3 may function in the epigenetic regulation of gene expression and facilitate transcriptional response to myocardial infarction (Olsen et al. 2017). NEIL3 mRNA expression is increased in human carotid plaques and Neil3 deficiency accelerates plaque formation in Apoe knockout mice, but it appears that this is not correlated with oxidative DNA damage (Skarpengland et al. 2016).The function of NEIL3 in removal of hydantoins from single strand DNA may be important for removal of replication blocks in proliferating cells. Mouse embryonic fibroblasts and neuronal stem cell derived from Neil3 knockout mouse embryos show decreased proliferation capacity and increased sensitivity to DNA damaging agents (Rolseth et al. 2013). NEIL3 may be required for maintenance of adult neurogenesis, as Neil3 knockout mice exhibit learning and memory deficits and synaptic irregularities in the hippocampus (Regnell et al. 2012). In addition, NEIL3 deficient neuronal stem cells exhibits signs of premature senescence (Reis and Hermanson 2012) and Neil3 knockout mice show reduced ability to augment neurogenesis to repair damage induced hypoxia ischemia (Sejersted et al. 2011).Mice that are triple knockout for Neil1, Neil2 and Neil3 do not show a predisposition to tumour formation or changes in telomere length (Rolseth et al. 2017).