Abstract The differentiation process of Hematopoietic Stem Cells (HSC) to Common Lymphoid Progenitors (CLP), that give raise to dendritic, NK, B and T cells, depends on various cues received from their microenvironment. Notch-1 is a transmembrane receptor that plays a crucial role on CLP commitment towards T cell lineage at the expense of B cell fate. The role of the transcription factor GATA-3, as well as its regulatory interaction with Notch-1 signals during early T cell development, is poorly characterized. In vitro studies show that GATA-3-deficient (GATA-3-/-) T cell progenitors do not develop beyond the CD44+CD25+ double negative 2 (DN2) stage. Remarkably, GATA-3-/- DN2 cells generate B cells in the presence of constant Notch-1 signals, which normally block B cell development. These GATA-3-/- DN2 cell express elevated levels of Deltex-1, a Notch-1 regulator. Therefore, we hypothesize that GATA-3 transcriptional activity controls the expression of Deltex-1 and possibly other Notch-1 regulators. The expression levels of various regulators of Notch-1 in wild type and GATA-3-/- T cell progenitors will be evaluated using quantitative PCR. The effect of GATA-3 deficiency on the expression level of various genes involved in Notch signaling will be evaluated by qPCR array. Revealing the interaction mechanism of GATA-3 with Notch-1 will contribute to our understanding of how early lymphocyte progenitors become committed toward the T cell lineage.