tem, where distal lung tissue from E18.5 Glucocorticoid Receptor (GR)–null mice have been exposed to at-RA. Whole genome microarrays and quantitative Real-time PCR have been utilized to identify and confirm GR-antagonised RA-responsive genes. Only the common rarb2/4 transcript and tcf15 (paraxis) were found to match this criteria. We propose that the antagonistic effects on alveolarisation by GC and RA are regulated by signaling through the rarb2/4-promoter. Furthermore, the transcriptional activation of some RA-responsive genes was dependent on the presence of GR. These genes include the RA-metabolising enzymes cyp1a1 and cyp7b1, the tight junction proteins cldn5 and cldn4 and the ECM-protein eln. These studies will provide a better understanding of the processes involved in alveolar development and the specific roles of GCand RA-signaling. These findings may impact on the procedures used in the care of premature infants, and hence reduce the effects of respiratory distress syndrome.