Under stress conditions such as infection, inflammation, and hematopoietic 
recovery following chemotherapy or transplantation, the hematopoietic system is 
required to meet the increasing demands, especially from myeloid cells. 
Therefore, an understanding of the molecular mechanism underlying stress 
hematopoiesis is clinically imperative. We previously showed that C/EBPβ, which 
is a transcription factor required for emergency granulopoiesis, plays a pivotal 
role at the level of hematopoietic stem/progenitor cells under stress 
conditions. Upon exposure to stress, the C/EBPβ protein is upregulated in the 
hematopoietic stem cells. A close examination of C/EBPβ knockout mice revealed 
that C/EBPβ regulates the proliferation and differentiation of hematopoietic 
stem cells at the cost of the self-renewing activity. Further elucidation of the 
functions and regulation of C/EBPβ in hematopoietic stem cells will facilitate 
an understanding of stress hematopoiesis.