During blood cell development, hematopoietic stem cells generate diverse mature 
populations via several rounds of binary fate decisions. At each bifurcation, 
precursors adopt one fate and inactivate the alternative fate either 
stochastically or in response to extrinsic stimuli and stably maintain the 
selected fates. Studying of these processes would contribute to better 
understanding of etiology of immunodeficiency and leukemia, which are caused by 
abnormal gene regulation during the development of hematopoietic cells. The 
CD4(+) helper versus CD8(+) cytotoxic T-cell fate decision serves as an 
excellent model to study binary fate decision processes. These two cell types 
are derived from common precursors in the thymus. Positive selection of their 
TCRs by self-peptide presented on either MHC class I or class II triggers their 
fate decisions along with mutually exclusive retention and silencing of two 
coreceptors, CD4 and CD8. In the past few decades, extensive effort has been 
made to understand the T-cell fate decision processes by studying regulation of 
genes encoding the coreceptors and selection processes. These studies have 
identified several key transcription factors and gene regulatory networks. In 
this chapter, I will discuss recent advances in our understanding of the binary 
cell fate decision processes of T cells.