Retinoic acid receptors (RARs) are critical transcriptional regulators that are involved in the development and differentiation of a wide variety of different cells (Evans 1988). Several lines of evidence suggest that RARs may be involved in the regulation of hematopoiesis. RARs (particularly RARα) are expressed in virtually all hematopoietic cell types (de The et al., 1989). Moreover, in acute promyelocytic leukemia (APL) patients that harbor the 15/17 chromosome translocation generating the aberrant RARα fusion transcript (designated PML-RARα), RA induces terminal granulocytic differentiation of the leukemia cells (Huang et al. 1988; Castaigne et al., 1990; Warrell et al., 1991). Our laboratory has been studying the role of retinoic acid (RA) and the RA receptors (RARs) in regulating various aspects of hematopoiesis. Our approach has involved introducing a dominant negative RA receptor construct into certain cell lines representing different hematopoietic lineages as well as into normal mouse bone marrow and then assessing any phenotypic changes in these transduced cells. We have constructed a retroviral vector (designated LRARα403SN), which harbors RARα with a COOH terminal truncation (Figure 1). We have observed that this construct exhibits dominant negative activity against the normal RARα in both mouse NIH3T3 cells and the HL-60 myeloid leukemia cell line (Tsai et al., 1992).