As immunoblotting procedures confirmed that Ctx-induced phospho-activation of FGFR3 was accompanied by increased steady-state FGFR3 protein expression (data not shown), our findings confirm and extend a recent study by Ware et al (2010) demonstrating that NSCLC cell lines rapidly acquire resistance to EGFR TKIs and Ctx through transcriptional de-repression of FGFR2 and FGFR3 expression. This evidence concerns the gene CYP27A1 and non-small cell lung carcinoma.