In the study of Oh et al., it has been shown that Notch2 and Notch1 are coexpressed within lymphoid-primed multipotent progenitor cells and CLPs; as the progenitor cells move toward T cell specification, Notch1 becomes the predominant receptor in double-negative T progenitor cells, corroborating with the finding that hematopoietic Notch1 deletion led to T cell deficiency (Radtke et al., 1999). This evidence concerns the gene NOTCH1 and congenital T-cell immunodeficiency.