GZMB and asthma: 1999; Christodoulopoulos et al. 2000; Sousa et al. 2000; Pujols et al. 2004; Goleva et al. 2006). These studies also indicate that increased expression of the nonfunctional GRβ isoform may account for glucocorticoid insensitivity in inflammatory diseases, among them asthma (Leung et al. 1997; Hamid et al. 1999; Sousa et al. 2000; Goleva et al. 2006). We can therefore hypothesize that TGFβ‐transdifferentiated myofibroblasts from WI‐38 cell line present a resistance to glucocorticoid treatment.