To evaluate the therapeutic potential of splicing modulation in drug-resistant ALL, we first determined the response to pladienolide B (Plad-B) in a T-ALL cell line CCRF-CEM-WT and three Dex-resistant CEM sublines: CEM/R30dm (unknown mechanism of Dex resistance), CEM-R5 and CEM-R5C3 (both characterized by defective GR function). Here, NR3C1 is linked to acute lymphoblastic leukemia.