Glucocorticoids (GC) are pivotal agents used in the treatment of childhood acute lymphoblastic leukaemia (ALL) but the molecular basis of GC-resistance remains unclear. Although mutation or loss of the glucocorticoid receptor (GR) leads to GCresistance in vitro, genetic aberration of the GR is rare in clinical samples. Expression-array studies have shown that commonly-upregulated genes associatec with GC-sensitivity include GR, glucocorticoid-induced leucine zipper (GILZ) and kBa, which negatively interact with components of the pro-survival NFkB pathway and may be critical determinants of GC-sensitivity.