NANOG is a transcription factor in embryonic stem cells (ESCs) and is thought to be a key factor in maintaining pluripotency. NANOG is thought to function in concert with other factors such as POU5F1 (Oct-4) and SOX2 to establish ESC identity. These cells offer an important area of study because of their ability to maintain pluripotency. In other words, these cells have the ability to become virtually any cell of any of the three germ layers (endoderm, ectoderm, mesoderm).  It is for this reason that understanding the mechanisms that maintain a cell's pluripotency is critical for researchers to understand how stem cells work, and may lead to future advances in treating degenerative diseases.
NANOG has been described to be expressed in the posterior side of the epiblast at the onset of gastrulation. There, NANOG has been implicated in inhibiting embryonic hematopoiesis by repressing the expression of the transcription factor Tal1. In this embryonic stage, NANOG represses Pou3f1, a transcription factor crucial for the anterior-posterior axis formation.
Analysis of arrested embryos demonstrated that embryos express pluripotency marker genes such as POU5F1, NANOG and Rex1.  Derived human ESC lines also expressed specific pluripotency markers:
*TRA-1-60
*TRA-1-81
*SSEA4
*alkaline phosphatase
*TERT
*Rex1
These markers allowed for the differentiation in vitro and in vivo conditions into derivatives of all three germ layers.
POU5F1, TDGF1 (CRIPTO), SALL4, LECT1, and BUB1 are also related genes all responsible for self-renewal and pluripotent differentiation.
The NANOG protein has been found to be a transcriptional activator for the Rex1 promoter, playing a key role in sustaining Rex1 expression. Knockdown of NANOG in embryonic stem cells results in a reduction of Rex1 expression, while forced expression of NANOG stimulates Rex1 expression.
Besides the effects of NANOG in the embryonic stages of life, ectopic expression of NANOG in the adult stem cells can restore the proliferation and differentiation potential that is lost due to organismal aging or cellular senescence.