Nuclear Factor kappa B (NF-kB) is a family of transcription factors that participates in the regulation of cell proliferation, migration, and apoptosis. Impaired NF-kB activity appears to be involved in the pathophysiology of inflammatory states, autoimmune diseases, and cancer.

Genetic manipulation in mice leading to impaired NF-kB function is associated with abnormal limb development and delayed bone growth. We have previously shown in rodent cultured chondrocytes and cultured metatarsal bones that NF-kB promotes longitudinal bone growth and growth plate chondrocyte function. These NF-kB growth-promoting effects appear to be facilitated by Growth Hormone (GH) and Insulin-like Growth factor-1 (IGF-1). These stimulatory effects of GH and IGF-1 on NF-kB activity are supported by observational evidence in humans; a number of individuals carrying mutations that alter NF-kB function exhibit growth failure and GH insensitivity.

核因子κB（NF-kB）是转录因子家族，参与细胞增殖，迁移和凋亡的调控。受损的NF-kB活性似乎与炎症，自身免疫性疾病和癌症的病理生理有关。

导致NF-kB功能受损的小鼠中的基因操作与肢体发育异常和骨骼生长延迟有关。我们先前已经在啮齿动物培养的软骨细胞和culture骨的培养物中表明，NF-kB促进了纵向骨生长和生长板软骨细胞功能。这些生长激素（GH）和胰岛素样生长因子1（IGF-1）似乎促进了这些NF-kB的生长促进作用。GH和IGF-1对NF-kB活性的这些刺激作用得到了人类观察证据的支持。许多携带可改变NF-kB功能的突变的个体表现出生长衰竭和GH不敏感。