We show that the mechanism of this drug combination involves downregulation of signal transducer and activator of transcription 6 (STAT6) and PDGF-associated protein 1 (PDAP1), which appear to function in a predictedSTAT6–ERK–NF-κB regulatory network that may be implicated in apoptosis resistance in childhood ALL. The gene discussed is NFKB1; the disease is acute lymphoblastic leukemia.