Glucocorticoid hormones stimulate Na⁺ transport in distal lung epithelial cells by increasing apical Na⁺ conductance (GNa⁾ (Ramminger et al., 2004) and such responses have been attributed to glucocorticoid receptor-mediated expression of the epithelial Na⁺ channel α-subunit (α-ENaC) gene (Sayegh et al., 1999). However, the glucocorticoid-evoked increases in Gseen in H441 distal Na airway cells are augmented by T₃ (Ramminger et al., 2004), which accords with the view that glucocorticoid and thyroid hormones are both important to the development of the lungs’ Na⁺ absorbing phenotype (reviewed by Olver et al., 2004). We have therefore explored the possibility that this effect of T₃ may reflect facilitation of glucocorticoid-evoked α-ENaC transcription (Otulakowski et al., 1999).Our control data confirmed (Otulakowski et al., 1999; Sayegh et al., 1999) that dexamethasone, a synthetic glucocorticoid, can activate the α-ENaC promoter and showed that half maximal activation occurred at ~5 nM (Fig. 1). However, T₃, at a concentration that can clearly augment the effect of dexamethasone upon G_Na(Ramminger et al., 2004), had no effect upon this response (Fig. 1). In contrast to earlier data from the rat α-ENaC promoter (Otulakowski et al., 1999), the present results suggest that, in human cells, the potentiating effect of T₃ (Ramminger et al., 2004) must reflect events downstream to transcription.