GATA1 and asthma: Retroviral transduction of human CD34+ hematopoietic progenitors with a GATA-1 expression vector selectively drives these myeloid progenitors to differentiate nearly exclusively into eosinophils [13], and transgenic deletion of a palindromic double GATA-1 binding site in the murine GATA-1 HS2 control locus, leads to an exclusive loss of the eosinophil lineage [14], providing a novel eosinophil-deficient mouse for studies of eosinophil effector function in the pathophysiology of asthma [15] and other eosinophil-associated diseases.