It is thought that this occurs by negating the effects of decreased phosphorylation and activation of USF-1 under IUGR conditions via activation of a signaling cascade culminating in the phosphorylation of many important pancreatic beta cell proteins, allowing for proper USF-1 binding to the PDX1 promoter region and the subsequent transcription of the all-important PDX1 protein product (Pinney et al., 2011). The gene discussed is PDX1; the disease is fetal growth restriction.