非酒精性脂肪肝（NAFLD）是临床高发疾病，肝脏脂肪酸氧化减少是其病理特征之一，然而其内在机制尚不明了。NF-κB诱导激酶（NIK）作为NF-κB通路的的上游组分，可能是上述现象的操控者。NIK在肥胖个体的肝脏中激活，可能通过降低PPARα的蛋白水平，阻遏受其转录调控的脂肪酸氧化酶基因，抑制了肝脏脂肪酸氧化，最终推动了NAFLD的发展。因此，NIK可能成为治疗NAFLD的新靶点。

Nonalcoholic fatty liver disease (NAFLD) has a high morbidity clinically, characteristic of reduced free fatty acid oxidation. However, the potential mechanism is not clear. NF-κB inducing kinase (NIK), the upstream of NF-κB pathway, may be the modulator of the reduction of oxidation metabolism. Hepatic NIK, enhanced in obesity, may reduce the protein level of PPARα, by which NIK inhibits the transcription of genes involved in free fatty acid oxidation. Thus hepatic free fatty acid oxidation is reduced by NIK, leading to the exacerbation of NAFLD. NIK may become the target for NAFLD therapy.