Treatment of hematological diseases such as leukemia and lymphoma rely on the transplantation of hematopoietic stem cells (HSCs) derived from limited numbers immune- compatible donors. Recent advances in stem-cell biology have enabled the generation of pluripotent stem cells (iPSCs) from terminally differentiated cells of healthy patient tissue. This provides the opportunity to generate bona fide HSCs, circumventing the limitations of donor- derived transplantation; however, inadequate knowledge of the innate molecular mechanisms hinders progress to this end. A key hematopoietic regulator in mammals, GATA2, is indispensable for HSC formation and maintenance. Therefore, dissection of its molecular mechanism and function in HSC development would be a crucial step in in vitro synthesis of HSCs. Unfortunately, GATA2 also maintains functional roles in endothelial development making it difficult to isolate its specific role towards HSC specification. Fortunately, recent studies have identified two paralogs of GATA2 in zebrafish, gata2b and gata2a, in which the hematopoietic and endothelial functions seem to have segregated. Using a comparative approach of the similarities shared between GATA2 and its paralogs, we can provide further insight into GATA2 function in HSC development. Our current studies have shown that gata2b and gata2a function in distinct manners. Furthermore, we have shown that mutations within the N-terminal zinc finger binding domain of GATA2 and its paralogs affect the function of the protein. These results indicate the gata2b zinc finger binding domain may result in its hematopoietic specific identity