Inducible inactivation of Notch1 led to T cell deficiency, which was transplantable when Notch1-deleted hematopoietic cells were engrafted into wild type (WT) recipients, demonstrating the cell autonomous role of Notch1 signaling in specifying T cell differentiation (Radtke et al., 1999). Here, NOTCH1 is linked to congenital T-cell immunodeficiency.