Having demonstrated that colayers of MSC cells could mimic the effect of PGE2, cAMP induction, or PKA agonists on p53 levels and cell death in BCP-ALL cultures [11], we proceeded to examine the hypothesis that prosurvival signalling from BM stroma could in part be mediated through signalling cascades involving the PGE2-cAMP-PKA axis. The gene discussed is TP53; the disease is acute lymphoblastic leukemia.